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Objective: To examine changes in cause-specific Years of Life Lost (YLL) by age, race, and sex group in the USA from 1990 to 2014. Methods: 60 million death reports from the National Center for Health Statistics (NCHS) were categorized by age group, sex, race, and cause of death. YLL were calculated using age-specific life expectancies. Age groups were: infants <1, children 1–19, adults 20–64, and older adults 65+. Results: Blacks have historically experienced more years of life lost than whites or other racial groups in the USA. In the year 1990 the YLL per 100,000 population was 21,103 for blacks, 14,160 for whites, and 7,417 for others. Between 1990 and 2014 overall YLL in the USA improved by 10%, but with marked variations in the rate of change across age, race, and sex groups. Blacks (all ages, both sexes) showed substantial improvement with a 28% reduction in YLL, compared to whites (all ages, both sexes) who showed a 4% reduction. Among blacks, improvements were seen in all age groups: reductions of 43%, 48%, 28%, and 25% among infants, children, adults, and older adults, respectively. Among whites, reductions of 33%, 44%, and 18% were seen in infants, children, and older adults, but there was a 6% increase in YLL among white adults. YLL increased by 18% in white adult females and declined 1% in white adult males. American Indian/Alaska Native women also had worsening in YLL, with an 8% increase. Asian Pacific Islanders consistently had the lowest YLL across all ages. Whites had a higher proportion of YLL due to overdose; blacks had a higher proportion due to homicide at younger ages and to heart disease at older ages. Conclusions: Race-based disparities in YLL in the USA since 1990 have narrowed considerably, largely as a result of improvements among blacks compared to whites. Adult white and American Indian / Alaskan Native females have experienced worsening YLL, while white males have experienced essentially no change. If recent trajectories continue, adult black/white disparities in YLL will continue to narrow. [ABSTRACT FROM AUTHOR]

Purpose: This study aims to better understand the individual characteristics and dietary factors that affect the relationship between estimated consumption of acrylamide and measured acrylamide hemoglobin adduct levels (HbAA) and glycidamide hemoglobin adduct levels (HbGA).Methods: Acrylamide levels in individual food items, estimated by the U.S. Food and Drug Administration, were linked to data collected in the 2003-2004 National Health and Nutrition Examination Survey. Multivariable linear regression was used to evaluate the relationship between estimated consumption of acrylamide and HbAA.Results: A significant association between acrylamide intake and HbAA was observed, after adjustment for gender, race/ethnicity, smoking status, age, and BMI (R2 = 0.34). Across quartiles of acrylamide consumption, HbAA and HbGA levels increased monotonically. Among nonsmokers, an evaluation of three heavily consumed, high AA concentration foods showed a positive trend between the consumed amount of fried potatoes and HbAA in children, adolescents, and adults. A significant positive trend between the consumed amount of potato chips or coffee was indicated in adolescents, adults, and seniors.Conclusions: Consumption of some individual foods affects HbAA concentrations more strongly and in an age-dependent manner. Our results suggest that effective dietary guidelines for controlling acrylamide intake should be subpopulation specific. [ABSTRACT FROM AUTHOR]

Objectives: To evaluate total and cause-specific mortality among hardmetal production workers with emphasis on lung cancer. Methods: Subjects were 7304 workers ever employed in one of eight US plants from 1952 to 2008. Vital status through 2012 was determined for 97% of subjects and cause of death for 98.3% of 1087 deaths. We computed standardized mortality ratios (SMRs) and evaluated exposure-response via relative risk regression analysis. Results: We observed overall deficits in deaths for total mortality, all cancers, and lung cancer and found no evidence of any exposure- response relationships for lung cancer. Conclusions: We found no evidence that exposure to tungsten, cobalt, or nickel, at levels experienced by the workers examined, increases lung cancer mortality risks. We also found no evidence that work in the US hardmetal industry increases mortality risks from any other causes of death. [ABSTRACT FROM AUTHOR]

Although blood lead levels (BLLs) in US children have dramatically declined over the past 40 years, there remain pockets of children living in areas with elevated BLLs. While some increases (≥ 10 μg/dL) may be associated with legacy lead paint, ambient air lead may be contributing to the problem. A deidentified dataset of information on over 60,000 Kansas children under 3 years of age who were tested for BLL was provided through the Kansas Environmental Public Health Tracking Network for the period 2000-2005. Using ArcGIS, we calculated distance (in miles) from a lead-emitting industry referred to as a toxic release inventory (TRI) site. The USEPA TRI database tracks the management of certain toxic chemicals that may pose a threat to human health. US facilities in different industry sectors must report annually amount of substances like lead into the environment including their exact location. Distance from a TRI site was inversely related to BLL after controlling for area-level poverty and pre-1950 housing. The results of our evaluation indicate there is a significant relationship between proximity to lead industry and childhood BLLs. Proximity to sources of lead emissions should be evaluated as a possible factor when identifying children for targeted BLL testing. [ABSTRACT FROM AUTHOR]

Introduction. Although lead paint and leaded gasoline have not been used in the US for thirty years, thousands of US children continue to have blood lead levels (BLLs) of concern. Methods.We investigated the potential association of modeled air lead levels and BLLs ⩾ 10 μg/dL using a large CDC database with BLLs on children aged 0-3 years. Percent of children with BLLs ⩾ 10 μg/dL (2000-2007) by county and proportion of pre-50 housing and SES variables were merged with the US EPA's National Air Toxics Assessment (NATA) modeled air lead data. Results.The proportion with BLL ⩾ 10 μg/dL was 1.24% in the highest air lead counties, and the proportion with BLL ⩾ 10 μg/dL was 0.36% in the lowest air lead counties, resulting in a crude prevalence ratio of 3.4. Further analysis using multivariate negative binomial regression revealed that NATA lead was a significant predictor of % BLL ⩾ 10 μg/dL after controlling for percent pre-l950 housing, percent rural, and percent black. A geospatial regression revealed that air lead, percent older housing, and poverty were all significant predictors of % BLL ⩾ 10 μg/dL. Conclusions. More emphasis should be given to potential sources of ambient air lead near residential areas. [ABSTRACT FROM AUTHOR]

Abstract: Three of us (G.M., A.Y., and P.M.) performed reanalyses of the National Cancer Institute cohort study on nasopharyngeal cancer (NPC) risk among formaldehyde exposed workers (). Both reanalyses () were published in this journal. However, the mortality follow-up performed by the NCI working group reported in two publications by was later stated to be incomplete (). This incomplete follow-up may impact the validity of the results of our reanalyses. At this time, corrected estimates for solid cancer mortality risks including NPC as reported in have not been provided as an erratum by the authors or reported anywhere else to our knowledge. We would like to inform readers about these issues and ask for a prompt corrigendum of the 2004 publication by the NCI working group since this study has played such a prominent role in causal evaluations. [ABSTRACT FROM AUTHOR]

The article discusses the study which updates the mortality experience of a cohort of workers with and without potential exposure to acrylamide (AMD) at three plants in the U.S. and one plant in the Netherlands. The standardized mortality ratio was computed using the national and local rates and modeled internal cohort rates to asses site-specific cancer risks by demographic and work history factors and several exposure indicators for AMD. The results of the study are also emphasized in the article.

The extensive data from the Blair et al.( ) epidemiology study of occupational acrylonitrile exposure among 25,460 workers in eight plants in the United States provide an excellent opportunity to update quantitative risk assessments for this widely used commodity chemical. We employ the semiparametric Cox relative risk (RR) regression model with a cumulative exposure metric to model cause-specific mortality from lung cancer and all other causes. The separately estimated cause-specific cumulative hazards are then combined to provide an overall estimate of age-specific mortality risk. Age-specific estimates of the additional risk of lung cancer mortality associated with several plausible occupational exposure scenarios are obtained. For age 70, these estimates are all markedly lower than those generated with the cancer potency estimate provided in the USEPA acrylonitrile risk assessment.( ) This result is consistent with the failure of recent occupational studies to confirm elevated lung cancer mortality among acrylonitrile-exposed workers as was originally reported by O'Berg,( ) and it calls attention to the importance of using high-quality epidemiology data in the risk assessment process. [ABSTRACT FROM AUTHOR]

Presents information on a study that evaluated the role of cigarette smoking in respiratory system cancer among fiberglass and rock/slag wool production workers in the United States. Methodology of the study; Results and discussion on the study; Conclusions.

Presents information on a study that evaluated the role of tobacco smoking in the excess of respiratory system cancer among fiberglass and rock/slag wool production workers in the United States. Methodology of the study; Results and discussion on the study; Conclusions.

Presents statistical computer programs in the United States. Availability of PCBRAP down-loaded version of the Bayesian Analysis Package; Methodologies used in the MUDIFT program for the distribution-free comparison of growth curves; Calculation of percentiles through PCT.

It is probable that most teachers of economics use the publications of the Federal Reserve Banks with their students. In this article, Cohen and Marsh report on an interesting systematic attempt to compare the effectiveness of Federal Reserve BankReviews with the effectiveness of the scholarly literature upon which the Review articles were based. Readers will be interested not only in their findings, but in the research design they utilized. [ABSTRACT FROM AUTHOR]

Reports on the mortality patterns among chemical plant workers exposed to formaldehyde and other substances. Development of nasopharyngeal cancer excess based on four cases from an American Cyanamid Co. chemical plant in Wallingford, Connecticut; Quantitative estimation of worker exposures for formaldehyde, product particulates and non-product particulates.

Complete and accurate ascertainment of vital status is of great importance in cohort studies. Recently, during the vital status ascertainment phase of an ongoing occupational mortality study, the authors discovered a potentially serious problem with use of the Pension Benefit Information Company's tracing service or any tracing that relies on records from the Social Security Administration (SSA) Death Master File to identify deaths. Their investigation revealed that a number of US states restrict the information in the SSA's Death Master File that is available to researchers and the public as a source of death information. As a result of these findings, the authors recommend a revised two-stage vital status tracing protocol. For stage I, data on all subjects for whom vital status is unconfirmed should be sent to the SSA. For stage II, information on all subjects to whom SSA assigned an unknown vital status as well as all subjects whom SSA identified as known decedents should be submitted to the National Death Index. This new protocol will enable researchers to maximize vital status ascertainment while containing costs associated with death identification. [ABSTRACT FROM AUTHOR]

The authors traced incidence of central nervous system cancer in a large occupational cohort of jet engine manufacturing workers from 1976 to 2004 in the 24 US states that comprised 95% of the cohort deaths. The cohort of approximately 224,000 employees was matched with cancer registry data; all central nervous system cancer matches were requested with their diagnostic data. This paper highlights the obstacles encountered while conducting this retrospective cancer incidence study. The authors spent approximately 700 hours completing applications and obtaining the cohort matches. Approximately 70% of the cases were identified in the state in which the facility of interest is located. In addition to the large amount of time involved, identified issues include complicated approval processes, high costs, temporal differences among the registries, and registry agency difficulty in performing the matching. Several states do not allow individual-level data to be used for research purposes. Researchers can gain important cancer incidence information by matching retrospective cohorts to multiple state cancer registries. However, they should carefully weigh the time and costs required and plan accordingly. Despite some serious obstacles, many of which are potentially resolvable, cancer incidence studies of retrospective cohorts using multiple cancer registries are feasible. [ABSTRACT FROM AUTHOR]

Discusses the findings of the exposure assessments of the United States man-made vitreous fiber production workers. Rationale for exposure evaluation and assignments; Sources of fiber exposure and co-exposures; Estimation of historic exposure intensities; Findings from company exposure data; Conclusions.

Background U.S. urban air quality has improved dramatically over the past decades. We evaluated acute effects of fine particulate matter (PM 2.5 ) on cardiovascular (CVD) mortality among residents of Allegheny County in SW Pennsylvania (1999–2011) using spatio-temporal modeling of air pollutants (AP) to reduce misclassification error in exposure assessment. Methods Spatio-temporal kriging of daily PM 2.5 and ozone (O 3 ) was used to produce daily exposure estimates at the residence ZIP code. Time-stratified case-crossover analysis was conducted to examine short-term effects of PM 2.5 on CVD mortality, adjusting for O 3 and apparent mean temperature. We studied both single and distributed lags for days 0–5. All CVD mortality and subcategories of ischemic heart disease (IHD), acute myocardial infarction, cerebrovascular disease, peripheral vascular disease (PVD), heart failure and cardiac arrhythmia were examined. Results A total of 62,135 deaths were identified. We found significant associations of PM 2.5 with IHD and PVD mortality at lag day 5: (2.1% (95% CI, 0.2–4.1%) and (7.6%, 95% CI, 0.05–15.7%) per 10 µg/m 3 increase of PM 2.5 in single lag models and for IHD in distributed lag models. There were no statistically significant associations with PM 2.5 for any of the other outcomes. Conclusions The application of finer scale geographically resolved AP exposures made it possible to study acute effects of PM 2.5 on CVD mortality in a large metropolitan area. Our study results demonstrated the continued presence of a dose response relationship of increased risk of CVD mortality within this lower range of PM 2.5 exposure. [ABSTRACT FROM AUTHOR]

Objectives: The purpose of this study was to examine US accidental poisoning death rates by demographic and geographic factors from 1979 to 2014, including High Intensity Drug Trafficking Areas.Methods: Crude and age-adjusted death rates were formed for age group, race, sex, and county for accidental poisonings (ICD 9th revision: E850-E869; ICD 10th revision: X40-X49) from 1979 to 2014 using the Mortality and Population Data System housed at the University of Pittsburgh. Rate ratios were calculated comparing rates from 2014 to 1979, overall, by sex, age group, race, and county. Joinpoint regression detected changes in trends and calculated the average annual percentage change (AAPC) as a summary measure of trend.Results: Drug poisoning mortality rates have risen an average of 6% per year since 1979. Increases are occurring in all ages 15+, and in all race-sex groups. HIDTA counties with the highest mortality rates were in Appalachia and New Mexico. Many of the HIDTA border counties had lower rates of mortality.Conclusions: The drug poisoning mortality epidemic is continuing to grow. While HIDTA resources are appropriately targeted at many areas in the US most affected, rates are also rapidly rising in some non-HIDTA areas. [ABSTRACT FROM AUTHOR]

Background and Objectives: Exposure to particulate matter (PM2.5) has been associated with increased cardiovascular outcomes, mediated by a hypothesized biological mechanism of systemic inflammation and oxidation. Although PM10 has been linked to inflammatory markers in a nationally representative sample (NHANES) using data from earlier cycles (1989-1994); no study has considered these relationships for PM2.5 in more recent time periods. We examined the association of ambient PM2.5 exposure and inflammatory markers in adult NHANES participants for cycles 2001-2008.Methods: We linked each of the adult NHANES participant's address with meteorological and modeled air pollution data for each census tract in conterminous United States. The effects of short and long term PM2.5 on C-reactive protein, white blood cells, fibrinogen and homocysteine were analyzed using multiple linear regression, adjusting for cardiovascular risk factors, temperature and ozone. SAS SURVEYREG was used to account for the complex survey design of NHANES.Results: In the overall population, no significant positive associations were noted for either short or long term PM2.5 exposures for any of the biomarkers after controlling for confounders. However, stronger associations were found among obese, diabetics, hypertensive and smokers. For every 10μg/m(3) increase in PM2.5, there was an increase of (a) 36.9% (95% CI: 0.1%, 87.2%) in CRP at annual average PM2.5 (adjusting for short term exposure) among diabetics (b) 2.6% (95% CI: 0.1%, 5.1%) in homocysteine at lag 0 among smokers.Conclusions: In a nationally representative sample of individuals we noted no overall association between PM2.5 and biomarkers of cardiovascular risk. However, sensitive subgroups manifested increases in these markers to PM2.5 exposure. Further studies should concentrate on the impact of PM2.5 on these biomarkers in those with multiple cardiovascular risk factors. [ABSTRACT FROM AUTHOR]

AbstractYouk, Ada O., Jeanine M. Buchanich, Jon Fryzek, Michael Cunningham, Gary M. Marsh. An ecological study of cancer mortality rates in high altitude counties of the United States. High Alt. Med. Biol.13:98–104.—To test the hypothesis that sustained, increased hemoglobin levels as measured by residence in high altitudes lead to an increase of malignant cancer deaths, we performed an assessment of U.S. cancer mortality rates for people residing in high altitude counties compared with those in counties with altitudes close to sea level. This included a graphical analysis of mortality rates for all cancers, female breast cancer, respiratory system cancer (RSC) and non-Hodgkin lymphoma (NHL), computation of standardized mortality ratios (SMRs) and Poisson regression modeling. Overall, our ecological evaluation showed statistically significantly reduced SMRs and rate ratios (RRs) for high altitude residents compared to sea level residents. For the causes of death categories examined, we found no evidence that persons residing in high altitude counties are at an elevated risk of cancer mortality compared with persons living close to sea level. Our results corroborate previous altitude studies of cancer mortality. [ABSTRACT FROM AUTHOR]

Presents information on a study that analyzed all jobs held by a cohort of United States man-made vitreous fiber production workers to determine airborne fiber exposure. Methodology of the study; Results and discussion on the study; Conclusions.

Objectives: The study aimed to determine whether the National Cancer Institute's (NCI) recent suggestion of associations between acrylonitrile (AN) exposure and mortality in lung and bladder cancer and pneumonitis is robust to alternative methods of data analysis., Materials and Methods: We used the Richardson method to indirectly adjust risk ratios (RRs) in relation to AN exposure for potential confounding by smoking and asbestos. We repeated key analyses omitting workers from Plant 4 to account for possible local, historical shipyard-related asbestos exposures., Results: The adjustment of lung cancer RRs for confounding by both smoking and asbestos and omitting Plant 4 workers yielded mostly decreased RRs and much less evidence of a positive association with cumulative AN exposure., Conclusion: Overall, our reanalysis provided little evidence to support NCI's suggestion of associations between AN exposure and mortality in lung and bladder cancer and pneumonitis., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Marsh and Kruchten.)

Objectives: To evaluate long-term mortality rates among aerospace material manufacturing workers as follow-up to an earlier observed excess of nephritis/nephrosis., Methods: Subjects were 2020 workers ever employed in the facility during 1963-2014. Vital status through 2014 was determined for all subjects and cause of death for 99.2% of 492 deaths. We computed standard mortality ratios (SMR) and internal relative risks., Results: SMRs for nephritis/nephrosis were unremarkable. We observed statistically significant elevated SMRs for kidney cancer among all workers and for the category "other lymphatic hematopoietic tissue cancer" (4/5 deaths from multiple myeloma) among long-term workers with potential plant exposure., Conclusions: We found no evidence of elevated mortality rates for nephritis/nephrosis. Study limitations precluded robust evaluation of whether the elevated rates for kidney cancer and other lymphatic hematopoietic tissue cancer were related to occupational factors at the study site. Our findings for these two cancers warrant continued mortality follow-up., (© 2019 Wiley Periodicals, Inc.)

Background: There has been no investigation to date of adults with metabolic syndrome examining the association of short and long-term exposure to fine particulate matter (PM 2.5 ) air pollution with cardiovascular-disease related inflammatory marker (WBC and CRP) levels in a nationally representative sample. The goal of this study is to assess the susceptibility of adults with metabolic syndrome to PM 2.5 exposure as suggested by increased cardiovascular-disease related inflammatory marker levels., Methods: A cross sectional analysis of adult National Health and Nutrition Examination Survey (NHANES) participants (2000-2008) was carried out with linkage of CDC WONDER meteorological data and downscaler modeled USEPA air pollution data for census tracts in the continental United States. Participants were non-pregnant NHANES adults (2000-2008) with complete data for evaluating presence of metabolic syndrome and laboratory data on WBC and CRP. Exposures studied included short (lags 0-3 days and their averages), long-term (30 and 60 day moving and annual averages) PM 2.5 exposure levels at the census tract level in the continental United States. The main outcomes included CRP and WBC levels the day of NHANES study visit analyzed using multiple linear regression, adjusting for age, gender, race, education, smoking status, history of any cardiovascular disease, maximum apparent temperature and ozone level, for participants with and without metabolic syndrome., Results: A total of 7134 NHANES participants (35% with metabolic syndrome) met the inclusion criteria. After adjusting for confounders, we observed a significant effect of PM 2.5 acutely at lag day 0 on CRP level; a 10µg/m 3 rise in lag day 0 PM 2.5 level was associated with a 10.1% increase (95% CI: 2.2-18.6%) in CRP levels for participants with metabolic syndrome. For those without metabolic syndrome, the change in CRP was -1.3% (95% CI -8.8%, 6.8%). There were no significant associations for WBC count. In this first national study of the effect of PM 2.5 air pollution on levels of cardiovascular-disease related inflammatory markers in adults with metabolic syndrome, CRP levels were found to be significantly increased in those with this condition with increased fine particulate matter levels at lag day 0. With one third of US adults with metabolic syndrome, the health impact of PM 2.5 in this sensitive population may be significant., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Objectives: To update a cohort study of chemical workers and reevaluate lung cancer mortality in relation to acrylonitrile (AN) exposure., Methods: Subjects were 2096 workers employed during 1955 to 2011. We identified 474 deaths through 2011, and quantitatively estimated worker exposures to AN. Analyses included national and county-based standardized mortality ratios and relative risk regression of internal cohort rates., Results: We found no statistically significant excess mortality risks associated with Lima employment for any cause of death category, including lung cancer and other cancer sites implicated in previous studies., Conclusions: This update provides no evidence that exposure to AN at levels experienced by Lima workers is associated with an increased risk of lung cancer mortality, as suggested in original study. Earlier reported bladder cancer risks decreased to a much lower, not statistically significant level.

Purpose: To compare ascertainment of central nervous system (CNS) neoplasms with the use of mortality and incidence data as part of an occupational epidemiology study., Methods: Deaths were identified by matching the cohort of 223,894 jet engine manufacturing employees to the U.S. Social Security Administration death files and the National Death Index. Incident cancer cases were identified by matching the cohort to 19 state cancer registries., Results: We identified 718 cases overall: 59% by the use of both mortality and cancer incidence tracing; 24% by the use of only mortality tracing, and 17% by the use of only cancer incidence tracing. Compared with state cancer registries, death certificates missed 38% of the malignant, more than six times the benign and nearly 1.5 times the unspecified CNS cases. The positive predictive value of death certificates, with cancer registry as gold standard, was 6% for unspecified, 35% for benign, and 86% for malignant histologies., Conclusions: Death certificates seriously underascertained benign and unspecified CNS tumors; analyses determined with mortality data would not accurately capture the true extent of disease among the cohort. Most state cancer registries have only collected nonmalignant CNS tumor information since 2004, which currently limits the usefulness of state cancer registries as a source of nonmalignant CNS tumor identification. Underascertainment of CNS deaths could seriously affect interpretation of results, more so if examining nonmalignant CNS., (Copyright © 2010 Elsevier Inc. All rights reserved.)

Objective: To explore a perceived unusual occurrence of glioblastoma at one jet engine manufacturing facility located in North Haven (NH), Connecticut (CT)., Methods: Subjects were 212,513 workers ever employed in 1 of 8 manufacturing facilities from 1952 to 2001 and at risk from 1976 to 2004. We identified 722 cases of CNS neoplasms mainly by tracing through 19 state cancer registries. We computed standardized incidence ratios (SIRs) based on CT state and national rates and modeled internal relative risks (RRs)., Results: We found overall deficits in cases for glioblastoma (275 cases, SIR = 0.77, CI = 0.68-0.87) and most other histology categories examined. NH workers had a not statistically significant overall 8% excess in glioblastoma (43 cases, SIR = 1.08, CI = 0.78-1.46). Salaried NH workers had a statistically significant twofold risk of glioblastoma compared with hourly workers (17 cases, RR = 2.04, CI = 1.15-3.57). Other subgroups of NH workers revealed elevated but not statistically significant glioblastoma risks but little evidence of an association with duration of employment or time since first employment., Conclusions: Incidence rates for glioblastoma and other malignant CNS neoplasm histologies were not elevated in the total cohort. The glioblastoma excesses observed among NH workers may reflect external occupational factors, non-occupational factors or workplace factors unique to NH unmeasured in the current study., (Copyright 2010 S. Karger AG, Basel.)

In a four-facility occupational epidemiology study of chloroprene monomer and polymer production workers, the chloroprene (CD) and vinyl chloride monomer (VCM) exposures were modeled for plant specific job title classes. In two facilities an acetylene-based process was used and in the other two plants only a butadiene-based process was used in the monomer synthesis. In the Acetylene process VCM was an undesirable by-product to be removed. In the newer butadiene-based process, VCM was not involved and the exposures to CD were considerably lower than they were in the earlier years. One of the limiting factors was the operator rotation within a number of job titles. This rotation and inability to differentiate between job titles subsumed in job classifications recorded in the work histories required an exposure classification scheme based on an order of magnitude separation of exposure classes. In the four facilities with considerable variation in the mix of the production methods, the CD exposures were remarkably similar in both calculated and measured values. The reductions in exposures were much more dependent upon the improvement of the production methods, rather than deliberate exposure control for occupational hygiene considerations. This is reasonable since the exposures were generally lower than the coeval exposure limits and/or guidelines. The estimated exposures were less than 100 ppm in the pre-1960 era and less than 10 ppm in the 1960-1980 era, less than 1 ppm 1980-1990 era and less than 0.5 ppm thereafter. The exposures were categorized in four classes for VCM and six classes for CD. The characteristic class exposure values were used to cumulate individual exposures over time with a quantification of the potential range for exposures that are reasonably certain to ascribe correct ranking to job classes.

Purpose: To examine mortality among workers in a pharmaceutical production plant and to address community concerns about 1980 to 1990 increases in local county cancer mortality rates., Methods: Subjects were 1999 workers with some full-time employment during the period between 1970 and 1996. We identified deaths through the year 2000 and reconstructed exposures to nine chemical agents with available exposure measurements. Data analyses included standardized mortality ratios (SMRs) and time trends in local cancer mortality rates., Results: We observed deficits in deaths from all causes combined, all cancers combined, and most cause of death categories examined. Male workers with potential plant exposure had excesses in deaths from all lymphatic-hematopoietic tissue cancers (LHTC), in particular non-Hodgkin's lymphoma (NHL), and respiratory system cancers (RSC) that were larger among long-term workers, but the pattern of findings suggested the excesses were probably not related to occupational factors at the plant. The increase in local county cancer mortality rates was simply the upward cycle of a periodic trend that peaked in 1990 and returned to 1980 levels in 2000., Conclusions: With the possible exceptions of LHTC, in particular NHL, and RSC, this study provided no evidence of elevated total or cause-specific cohort mortality risks. It does not appear that plant factors played a role in the 1980 to 1990 increases in local county cancer mortality rates.

Objective: To determine whether the National Cancer Institute's (NCI) recent suggestion of a causal association between formaldehyde exposure and mortality from leukemia and myeloid leukemia (ML) is robust with respect to alternative characterizations and categorizations of formaldehyde exposure and to alternative methods of data analysis., Methods: The original authors provided the cohort data. We computed US and local county rate-based standardized mortality ratios (SMRs) and internal cohort rate-based relative risks (RR) by categories of four formaldehyde exposure metrics (highest peak, average intensity (AIE), cumulative, and duration), using both NCI categories and an alternative categorization based on tertiles of deaths from all leukemia among exposed subjects. For highest peak exposure, we computed RRs by the duration of time worked in the highest peak category and the time since highest peak exposure. For AIE, we computed RRs by the duration of exposure and the time since first exposure., Results: Our external comparisons revealed that the elevated leukemia and ML RRs and associated trends reported by NCI for highest peak and AIE occurred because null (or slight) to moderate mortality excesses were compared with statistically significant baseline category deficits in deaths. Our alternative categorization of AIE yielded leukemia and ML SMRs close to 1.0 in the highest exposure category, and revealed weaker evidence of a trend in RRs for leukemia and ML. We corroborated NCI's finding of no association for cumulative and duration of formaldehyde exposure. We found no consistent evidence that leukemia or ML risks increased with increasing duration of time spent in a given highest peak exposure (or for AIE, duration of exposure in a given AIE category). We also found no consistent evidence that leukemia or ML risks were greater in the more relevant shorter (less than 20 years) versus longer (20+ years) periods of time from the first highest peak exposure (or for AIE, first exposure)., Conclusions: Our reanalysis provided little evidence to support NCI's suggestion of a causal association between formaldehyde exposure and mortality from leukemia and ML. NCI's key findings for highest peak exposure and AIE do not adequately account for the inordinately large deficits in deaths in the categories used as the baselines for internal rate-based RRs. The NCI findings also do not adequately account for the duration of time subjects spent in the highest peak category (or for AIE, duration of exposure) or the time since their first peak exposure (or for AIE, time since first exposure). Our finding that NCI's suggestion of a causal association is not robust with respect to alternative categorizations of formaldehyde exposure and methods of data analysis casts considerable additional uncertainty regarding the validity of this suggested association.

The extensive data from the Blair et al.((1)) epidemiology study of occupational acrylonitrile exposure among 25460 workers in eight plants in the United States provide an excellent opportunity to update quantitative risk assessments for this widely used commodity chemical. We employ the semiparametric Cox relative risk (RR) regression model with a cumulative exposure metric to model cause-specific mortality from lung cancer and all other causes. The separately estimated cause-specific cumulative hazards are then combined to provide an overall estimate of age-specific mortality risk. Age-specific estimates of the additional risk of lung cancer mortality associated with several plausible occupational exposure scenarios are obtained. For age 70, these estimates are all markedly lower than those generated with the cancer potency estimate provided in the USEPA acrylonitrile risk assessment.((2)) This result is consistent with the failure of recent occupational studies to confirm elevated lung cancer mortality among acrylonitrile-exposed workers as was originally reported by O'Berg,((3)) and it calls attention to the importance of using high-quality epidemiology data in the risk assessment process.

An historical cohort study was conducted of workers at a pharmaceutical manufacturing plant. The cohort mortality experience of workers ever employed at the plant over the period from 1950 to 1999 was examined. The 1958 workers accumulated 44,294 person-years of experience at the plant, and a total of 384 deaths were identified. Our findings from external comparisons based on standardized mortality ratios (SMRs) in the cohort provide no evidence of excess mortality risk from all causes combined (SMR=0.75), all cancers combined (SMR=0.96), or from certain other individual causes of death. No patterns of excess mortality risk were apparent after stratifying on age and sex or job classification. The mortality experience of this cohort was generally more favorable than that of the general population.

We report the 1946-1992 mortality experience of 4008 females employed in any of 10 U.S. fiberglass manufacturing plants between 1945 and 1978 relative to external population rates. We also examine respiratory system cancer (RSC) mortality as a function of estimated exposure to respirable fibers (RFib), formaldehyde (FOR), silica, phenolics, urea, and other agents based on internal cohort comparisons. No statistically significantly elevated standardized mortality ratios were observed for all-cause mortality (930 deaths), any of the 25 nonmalignant causes considered, all malignant neoplasms (266 deaths), or any of the 27 malignant causes considered. Internal cohort comparisons revealed no significant positive associations between RSC mortality (53 cases) and exposure to RFib, FOR, or any of the other agents considered, although exposure levels were generally low. Some demographic subgroups appear to be at relatively increased risk of RSC.

Background: Because inherent variability may exist in data collected by multiple reviewers or from potential difficulties with data abstraction tools, we developed a standardized method of evaluating interrater reliability (IRR) for clinical studies, HEDIS effectiveness of care measures, and onsite/medical record reviews., Objective: To demonstrate the ability of our standardized methods of data collection and analysis of results to determine the extent of agreement between multiple reviewers; identify areas for improvement in data collection procedures; and improve data reliability., Study Design: A prospective chart review with concurrent IRR., Methods: A subsample of patient records included in the Highmark Blue Cross Blue Shield/Keystone Health Plan West basic medical review for each HEDIS measure was selected for the IRR study. An experienced nurse ("gold standard") conducted a blinded concurrent review of these records. Using the kappa statistic (kappa) we evaluated interobserver agreement between results of the onsite reviewers and the "gold standard" from 1997 through 2000. Revised data collection methods and enhanced reviewer training were incorporated for measures showing areas for rater improvement., Results: Results across years showed excellent IRR for most measures; however, each year 1 or 2 measures showed areas for rater improvement (1997 Papanicolaou kappa = 0.50; 1998 well-child visits 3 to 6 years kappa = 0.37; 1999 comprehensive diabetes kappa = 0.73; high blood pressure kappa = 0.73). After reevaluating these measures, the results of the kappa showed excellent interrater agreement in subsequent years., Conclusions: Standardized methods of data collection and evaluation of IRR results provides health plans increased confidence in data collection, statistical analyses, and in reaching conclusions and deriving relevant recommendations.