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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 A retrospective cohort mortality study evaluated ischemic heart disease (IHD) among workers in the “rubber chemicals” manufacturing department of a Western New York plant. A previous study at the plant found elevated chest pain and angina among workers in this department. Methods Mortality experience of workers employed from 1946–1988 was followed through December 31, 1994. Mortality was compared to U.S. population rates and to local Niagara county rates by using the NIOSH life table analysis system. Poisson regression was used to examine patterns of IHD within the cohort. Results The standardized mortality ratio (SMR) for IHD among workers in the rubber chemicals department was 1.51 (U.S. rates) and 1.19 (Niagara county rates). Increased mortality from IHD in the rubber chemicals department was most pronounced at younger ages (

Concern is raised by Dobie [J. Acoust. Soc. Am. 103, 2734 (1998)] regarding a recent analysis [, J. Acoust. Soc. Am. 101, 950–963 (1997)] of the NIOSH Occupational Noise and Hearing Survey data. Specifically, issues are raised concerning (1) definition of hearing handicap, (2) the use of frequency-specific articulation index (AI) weights applied to the binaural pure-tone average of 1, 2, 3, and 4 kHz, and (3) conclusions regarding significant excess risk based on this definition. We have reviewed the development of the definitions of hearing handicap and provide additional support for the use of a hearing handicap definition based on the binaural pure-tone average of 1, 2, 3, and 4 kHz and the weighting of specific frequencies. Furthermore, our definition of noise-induced hearing handicap is similar to one of several proposed by the International Standards Organization (Reference 1999Reference 1990) and the American National Standards Institute (Reference 3Reference 44Reference 1996). Additional analyses show that there is significant evidence of excess risk at daily exposure levels below 85 dB using any of the pure-tone average and/or weighting strategies we have examined. Hence we have provided additional support for our conclusions regarding exposure-response curves and we have reaffirmed that our methods are appropriate for the scope of our analysis.

The regulation of hazards is one of the most dramatic forms of intervention in occupational safety and health (OSH). Despite their high degree of potential social and economic impact, relatively little research has been conducted to specifically evaluate the effectiveness of OSH standards with regard to preventing occupational diseases and injuries. This paper reviews the basic scientific approaches that may be used to evaluate the efficacy of OSH standards. These approaches encompass the following research areas: (1) exposure surveillance, (2) disease surveillance, and (3) prospective studies following the introduction of the standard. Research on asbestos and asbestosis, respirable crystalline silica (quartz) and silicosis, and respirable coal mine dust and coal workers' pneumoconiosis (CWP) are used to illustrate these approaches and the type of information that is currently available. The examples (quartz coal dust, asbestos) reveal substantial limitations in the types of information currently available for evaluating the efficacy of these OSH standards. Ideally, plans for evaluating the efficacy of OSH standards should be developed for existing and future standards. These plans should include programs for the surveillance of exposures and adverse health effects and, when possible, for prospective studies designed to evaluate how the risk of disease (or injury) is modified by the introduction of the standard. (This article is a US Government work and, as such, is in the public domain in the United States of America.) © 1996 Wiley-Liss, Inc.

Noise assessments have been conducted using full-shift dosimetry and short-term task-based measurements. Advantages of the task-based method include the opportunity to directly identify high-noise exposure tasks and to target control measures, as well as obtain estimates of task-based full-shift exposures; however, there is little empirical evidence comparing the two methods. National Institute for Occupational Safety and Health assessed noise exposures at three industrial facilities using dosimetry and task-based methods with the objective of comparing the two strategies and assessing the degree of agreement and causes of disagreement. Eight indices of task-based full-shift exposures were created from task-based sampling using three methods to assess time-at-task (direct observation by industrial hygienist, end-of-shift worker estimates and supervisor estimates) and three methods to assign noise levels to tasks [direct measurement, arithmetic mean (AM) and geometric mean (GM)]. We assessed aspects of agreement (precision, bias and absolute agreement) using Bland-Altman plots and concordance correlation coefficient (CCC). Overall, the task-based methods worked fairly well, with mean biases less than +/-2.8 dBA and precision ranges of 3.3-4.4 dBA. By all measures, task-based full-shift estimates based on supervisor assessment of time-at-task agreed most poorly with the dosimetry data. The task-based full-shift estimates based on worker estimates of time-at-task generally agreed as well as those based on direct observation. For task noise level, task-based full-shift estimates based on directly measured task agreed the best with dosimetry data, while agreement for task-based indices based on task AM or GM was variable. Overall, the task-based full-shift estimates based on direct observation task and direct measured task noise level achieved the best agreement with the dosimetry data (CCC 0.84) with 95% of their differences being within 7.4 dBA and 56% of the differences

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.

Methods for evaluating the hazards associated with noncancer responses with epidemiologic data are considered. The methods for noncancer risk assessment have largely been developed for experimental data, and are not always suitable for the more complex structure of epidemiologic data. In epidemiology, the measurement of the response and the exposure is often either continuous or dichotomous. For a continuous noncancer response modeled with multiple regression, a variety of endpoints may be examined: (1) the concentration associated with absolute or relative decrements in response; (2) a threshold concentration associated with no change in response; and (3) the concentration associated with a particular added risk of impairment. For a dichotomous noncancer response modeled with logistic regression, concentrations associated with specified added/extra risk or with a threshold responses may be estimated. No-observed-effect concentrations may also be estimated for categorizations of exposures for both continuous and dichotomous responses but these may depend on the arbitrary categories chosen. Respiratory function in miners exposed to coal dust is used to illustrate these methods.

We appreciate the opportunity to respond to comments by Valentgas and colleagues regarding our report examining mortality among rubber chemical manufacturing workers [Prince et al., 2001]. Following are our responses to their comments, focusing on the authors' main points

Studies indicate that the statistical properties and temporal structure of the sound signal are important in determining the extent of hearing hazard. As part of a pilot study to examine hearing conservation program effectiveness, NIOSH collected noise samples of impact noise sources in an automobile stamping plant, focusing on jobs with peak sound levels (Lpk) of greater than 120 dB. Digital tape recordings of sounds were collected using a Type I Precision Sound Level Meter and microphone connected to a DAT tape recorder. The events were archived and processed as .wav files to extract single events of interest on CD‐R media and CD audio media. A preliminary analysis of sample wavelet files was conducted to characterize each event using metrics such as the number of impulses per unit time, the repetition rate or temporal pattern of these impulses, index of peakedness, crest factor, kurtosis, coefficient of kurtosis, rise time, fall time, and peak time. The spectrum, duration, and inverse of duration for e...

This paper reviews the ISO‐1999 and ANSI S3.44 standards and the literature related to prediction of noise‐induced hearing loss (NIHL) in humans. The dearth of contemporary population‐based studies of hearing loss among industrial, low noise‐exposed individuals have made the ISO‐1999 and ANSI S3.44 standards a key source of comparative data for assessing the risk of NIHL. This paper will highlight how these standards have been used in several published papers to examine the magnitude of NIHL risk, predictions of noise‐induced thresholds in hearing conservation data, and to generate hypotheses regarding the biologic plausibility of hearing loss due to chemicals or other ototoxic agents.

Noise‐induced hearing loss (NIHL) has been recognized as a serious health concern for decades. ISO Standard 1999:1990 provides a means to predict noise‐induced hearing loss (NIHL) based on LAeq measurements in the working environments of workers. This standard seems to work well for predicting hearing loss in continuous noise fields. However, it is possible that ISO 1999 does not apply well to impact, impulsive, or other transient noise fields. NIOSH and University of Pittsburgh are currently developing noise‐sampling strategies to measure impact and impulse noise in a manufacturing environment with the aim of developing new impulsive noise metrics. As part of the study, broadband impact/impulse pressure measurements will be made. Issues such as instrumentation, data quality, repeatability, spatial sampling, equipment portability, and calibration are addressed. Also, the annotation, digitization, and editing of the waveforms will be discussed. As part of the project, an archival database of manufacturing ...

As part of a NIOSH study examining factors affecting hearing conservation program (HCP) effectiveness, a job‐noise exposure matrix was constructed using these data sources: (1) task‐based sound level survey data; (2) noise exposure data (dosimetry and sound level surveys) provided from plant historical reports; (3) information on process changes and engineering controls; (4) interviews with plant personnel (in engineering and safety departments); and (5) detailed work history data from personnel records for each employee in the plant HCP. For plants in which changes in exposures have occurred due to engineering control and process changes, exposure estimation becomes a challenge when there are data gaps in exposure and process changes. This paper discusses how data from structured employee interviews can be used in conjunction with available quantitative, records‐based data to reconstruct processes and machinery/layout history. The goal was to characterize how noise exposure determinants (manufacturing environment, equipment, processes, shift lengths) have changed and to estimate exposure by department, job, and era. The first step was to identify employees for interview whose jobs were located in departments where exposure data were sparse or nonexistent. Data collection efforts were then geared towards reconstructing noise exposure for specific departments and jobs over time.

NIOSH recommends that hearing loss prevention programs (HLPPs) be implemented for all workers whose unprotected 8‐h TWA exposures equal or exceed 85 dB and that the programs include at least the following components: (1) initial and annual audits of procedures, (2) noise exposure assessment, (3) engineering and administrative control of noise exposures, (4) audiometric surveillance and evaluation, (5) use of hearing protectors (for exposures >85 dB, regardless of duration), (6) education and motivation, (7) recordkeeping, and (8) program evaluation. All components except program evaluation and routine in‐hour audits are generally discussed in the Occupational Safety and Health Administration (OSHA) Hearing Conservation Amendment (HCA). This paper presents research approaches for systematically evaluating OSHA‐mandated hearing conservation programs. The intent of such research is to (a) develop methods for evaluating hearing conservation programs that can be used across several industrial sectors and (b) identify ways in which ‘‘hearing conservation’’ can effectively become ‘‘hearing prevention’’ programs. General approaches are presented for each program element and data collection issues are discussed with specific examples of how various methods can been used for program evaluation. The goal of such research strategies is to identify the best predictors of program effectiveness.

Analyses of data from the NIOSH Occupational Noise and Hearing Survey (OHNS) have previously focused on 1172 highly ‘‘screened’’ workers. This paper examines excess risk estimates for 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). Data are analyzed by age, duration of exposure, and sound level (8‐h TWA) for different definitions of noise‐induced hearing impairment. Hearing impairment was defined as a binaural average hearing threshold level greater than 25 dB at selected frequencies (1–4 kHz, 1–3 kHz, and 0.5, 1, and 2 kHz). The analysis suggests that excess risk estimates are sensitive to population characteristics as well as definition of impairment. Lifetime excess risk estimates for noise‐induced hearing impairment are similar for the unscreened and screened populations for 8‐h TWAs below 85 dB. However, compared to the unscreened population, higher excess risk estimates are observed for the screened population at A‐weighted levels greater than 85 dB. This difference in excess risk was most marked for hearing‐impairment definitions that include 3 and 4 kHz.

Several hearing conservation programs (n=15) from a cross‐section of U.S. industries were examined to test whether there are greater rates of change in hearing levels in relation to increasing cumulative noise exposure during the period of audiometric follow‐up. The analysis also examined whether rates of hearing loss were lower among workers who wear hearing protection relative to workers who do not. These 15 audiometric databases had a total of 15 794 workers with 62 095 audiograms. Differences in a linear combination of 1–4 kHz biaural hearing levels of consecutive audiometric tests were examined using mixed effects models to account for correlated, repeated observations on individuals. These differences were modeled as a function of cumulative noise, gender, race, hearing protection use, age, learning effects, and baseline hearing level (measured after 14 h of quiet time). Analyses were conducted for the combined and individual databases. The analysis indicates there is significant heterogeneity among...

Occupational hearing conservation programs (HCPs) have been implemented in many industries in accordance with the 1983 OSHA hearing conservation amendment. The availability of these longitudinal databases permits an examination of associations between changes in hearing levels with other variables, including noise exposure. This paper examined (1) whether there is an increased risk of NIHL from exposures below 85 dBA; (2) whether workers with noise exposures above 85 dBA who are required to use hearing protection still have an increased risk of NIHL compared to low‐noise‐exposed (less than 70 dBA) workers; and (3) how risk may depend on the type of hearing protection used and reported degree of compliance. The data used in this analysis include most of the data analyzed by the ANSI working group to examine hearing conservation program effectiveness. Variables included age, sex, race, type of hearing protection, industry code, and hearing threshold levels (for both ears, tested at 0.5, 1, 2, 3, and 6 kHz). Databases for comparison included both internal and external ‘‘control’’ groups with low‐noise exposure, as well as noise‐exposed populations in which either the hearing conservation program was highly effective and/or the population was well protected via good hearing protection compliance.

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)