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Gary M Marsh

Publications and source records attributed to Gary M Marsh.

At least 19 recordsLinked to original sources
PubMed2006

Mis-specified and non-robust mortality risk models for nasopharyngeal cancer in the National Cancer Institute formaldehyde worker cohort study.

An IARC (International Agency for Research on Cancer) working group categorized formaldehyde as a human carcinogen (Group 1) in 2004. A major component of the epidemiologic evidence evaluated by IARC to reach this decision was the analysis published by Hauptmann et al. [Hauptmann, M., Lubin, J. H., Stewart, P. A., Hayes, R. B., Blair, A. 2004. Mortality from solid cancers among workers in formaldehyde industries. Am. J. Epidemiol. 159, 1117-1130.] of the National Cancer Institute (NCI) historical cohort comprising industrial workers exposed to formaldehyde in 10 U.S. plants. The NCI authors emphasized the relationship found between highest formaldehyde peak exposure and death from nasopharyngeal cancer (NPC). We performed two additional types of re-analyses of the NCI cohort data with focus on peak exposure and NPC mortality. The analyses were aimed at (1) investigating whether the model specification chosen by Hauptmann et al. (2004) was appropriate (interaction assessment) and (2) exploring the degree of instability of the risk estimates for NPC in relation to highest peak exposure (sensitivity analysis). Hauptmann et al. (2004) failed to account for an important interaction structure between plant group and the exposure variable that prohibits a generalization of formaldehyde effects within the NCI cohort and, in particular, beyond the NCI cohort. In addition, our sensitivity analysis demonstrates considerable uncertainties in the risk estimates and points convincingly to instability problems particularly related to Plant 1. Even a simple sensitivity model taking only one additional death into account produced a variation of the risk estimates beyond the instability conveyed by standard confidence intervals. The results of our current reanalysis of the NCI study do not support NCI's suggestion of a causal association with formaldehyde exposure and nasopharyngeal cancer. The decision by the IARC working group to reclassify formaldehyde as a Group 1 substance was clearly premature considering: (1) the missing evidence of an NPC excess from the large British and NIOSH cohort studies; (2) the absence of an association with formaldehyde and NPC in the independent and expanded study of Plant 1; and (3) the mis-specified and non-robust internal analysis of the NCI cohort study brought to light in our current re-analysis. Thus, the 2004 IARC decision to reclassify formaldehyde as a Group 1 substance should be reconsidered.

Adenocarcinoma↗
PubMed2006

Classification of worker exposures.

The classification of jobs or workers by exposure is an important undertaking in any occupational epidemiological study. Hitherto, the exposure classification designs have been strongly motivated by a desire to generate a sufficient number of exposure classes for the determination of a potential exposure-response relationship. Thus, the partitioning of exposures has been more or less arbitrary. The misclassification problems created by the selection of an arbitrary number of exposure assignment classes have not been addressed. In any quantitative exposure classification scheme, specific job titles may be indistinguishable in existing employment records; therefore, between worker variability must be addressed when characterizing worker exposures. Also, industrial hygiene exposure measurements frequently used to characterize worker exposures are often treated as valid representations of exposures; but they are neither random nor systematic evaluations of worker exposures. As a result they do not represent sampling from the proper exposure stratification of workers. These observations suggest that the selection of exposure groups should be based on a more rigorous examination of the data and its limitations. Considering the probability of any given worker being placed into the proper class as the probability of finding the mean exposure for that worker within the class boundary, the general equations to quantify the misclassification rates for any classification design as well as the exposure class limits and their width for any acceptable misclassification rate are developed. If between worker variability could not be calculated from the available exposure measurements, then it might be estimated from the proper data compiled from the literature. By considering an acceptable level of exposure misclassification, it is possible to calculate the allowable number of exposure classes and the proper partitioning ratio for these classes. Thus, the trade-off between misclassification and number of exposure classes might be a satisfactory solution to this difficulty encountered in occupational epidemiology.

Empirical Research↗
PubMed2006

Chemical process based reconstruction of exposures for an epidemiological study. I. Theoretical and methodological issues.

In the occupational hygiene component of occupational epidemiological studies the goal is to assign group average exposure levels that can be used to compute individual cumulative exposures. This task requires the availability of sufficient amounts of proper individual exposure level data. Typically, the required data are either sparse, completely lacking or happenstance data collected for purposes not suitable for the aims of the study. In the epidemiological study of mortality patterns among industrial workers exposed to chloroprene and other substances, we developed and used a process analysis and modeling based exposure reconstruction to augment, extrapolate, or interpolate the available exposure data. The models developed utilize equations based on the engineering principles and chemistry associated with the processes as determined from the process documentation and task performance habits as determined from interviews of knowledgeable personnel. The resulting equations are tractable and provide a general basis for calculating exposure levels for vapors. The validation of the results with available exposure measurements suggests that comprehensive process analysis and modeling may be used to reconstruct exposures or to evaluate exposure potential with scientifically defensible methods. Furthermore, even in the absence of validating data, the methodology developed has potentially very useful applications in predicting exposure levels to newly synthesized substances. Properly interpreted, the limitations of modeling can be minimized to obtain scientifically reasonable results.

Chemical Industry↗
PubMed2006

Chemical process-based reconstruction of exposures for an epidemiological study. Part II. Estimated exposures to chloroprene and vinyl chloride.

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.

Chemical Industry↗
PubMed2006

Mortality patterns among industrial workers exposed to chloroprene and other substances. I. General mortality patterns.

We conducted an historical cohort study to investigate the mortality experience of industrial workers potentially exposed to chloroprene (CD) and other substances, including vinyl chloride (VC), with emphasis on cancer mortality, including respiratory system (RSC) and liver. In 1999, the International Agency for Research on Cancer (IARC) classified CD as a possible carcinogen (Group 2B); VC was classified in 1987 as a known human carcinogen (Group 1). Subjects were 12,430 workers ever employed at one of two U.S. industrial sites (Louisville, KY (n=5507) and Pontchartrain, LA (n=1357)) or two European sites (Maydown, Northern Ireland (n=4849) and Grenoble, France (n=717)), with earliest CD production dates ranging from 1942 (L) to 1969 (P). Two sites (L and M) synthesized CD with the acetylene process that produced VC exposures. We determined vital status through 2000 for 95% of subjects and cause of death for 95% of the deaths. Historical exposures for individual workers were estimated quantitatively for CD and VC. Workers ever exposed to CD ranged from 92.3% (M) to 100% (G); to VC from 5.5% (M) to 22.7% (L). We computed standardized mortality ratios (SMRs) (using national and regional standard populations) in relation to selected demographic, work history and exposure factors. We used worker pay type (white or blue collar) as a rough surrogate for lifetime smoking history. For the combined cohort, SMRs (95% CIs) for all causes combined, all cancers combined, RSC and liver cancer were, respectively, 0.72 (0.69-0.74), 0.73 (0.68-0.78), 0.75 (0.67-0.84) and 0.72 (0.43-1.13). Site-specific (L, M, P and G, respectively) SMRs were: for all cancers combined: 0.75 (0.69-0.80), 0.68 (0.56-0.80), 0.68 (0.47-0.95) and 0.59 (0.36-0.91); for RSC: 0.75 (0.66-0.85), 0.79 (0.58-1.05), 0.62 (0.32-1.09) and 0.85 (0.41-1.56); for liver cancer: 0.90 (0.53-1.44) (17 deaths), 0.24 (0.01-1.34) (1 death), 0.0 (0-2.39) (no deaths) and 0.56 (0.01-3.12) (1 death). Among all workers ever exposed to CD, SMRs were: for all cancers combined: 0.71 (0.66-0.76); for RSC: 0.75 (0.67-0.84); for liver cancer: 0.71 (0.42-1.14). We also observed no increased mortality risks among cohort subgroups defined by race, gender, worker pay type, worker service type (short/long term), time period, year of hire, age at hire, duration of employment, the time since first employment, and CD or VC exposure status (never/ever exposed). In summary, our study has many strengths and is the most definitive study of the human carcinogenic potential of exposure to CD conducted to date. We conclude that persons exposed to chloroprene or vinyl chloride at the levels encountered in the four study sites did not have elevated risks of mortality from any of the causes of death examined, including all cancers combined and lung and liver cancer, the cancer sites of a priori interest. This conclusion is corroborated by our detailed analyses of mortality in relation to qualitative and quantitative exposures to CD and VC at each of the four study sites, reported in our companion paper (Marsh et al., submitted for publication).

Adult↗
PubMed2006

Mortality patterns among industrial workers exposed to chloroprene and other substances. II. Mortality in relation to exposure.

As part of an historical cohort study to investigate the mortality experience of industrial workers exposed to chloroprene (CD) and other substances, including vinyl chloride monomer (VC), we analyzed mortality from all cancers combined, respiratory system (RSC) and liver cancer in relation to CD and VC exposures. Subjects were 12,430 workers ever employed at one of two U.S. sites (Louisville, KY (n=5507) and Pontchartrain, LA (n=1357)) or two European sites (Maydown, Northern Ireland (n=4849) and Grenoble, France (n=717)). Historical exposures for individual workers were estimated quantitatively for CD and VC. For sites L, M, P and G, respectively, average intensity of CD exposures (median value of exposed workers in ppm) were 5.23, 0.16, 0.028 and 0.149 and median cumulative exposures (ppm years) were 18.35, 0.084, 0.133 and 1.01. For sites L and M, respectively, average intensity of VC exposures (median value of exposed workers in ppm) was 1.54 and 0.03 and median cumulative exposures (ppm years) were 1.54 and 0.094. We performed relative risk (RR) regression modeling to investigate the dependence of the internal cohort rates for all cancers combined, RSC and liver cancer on combinations of the categorical CD or VC exposure measures with adjustment for potential confounding factors. We categorized exposure measures into approximate quartiles based on the distribution of deaths from all cancers combined. We also considered 5- and 15-year lagged exposure measures and adjusted some RR models for worker pay type (white/blue collar) as a rough surrogate for lifetime smoking history. All modeling was site-specific to account for exposure heterogeneity. We also computed exposure category-specific standardized mortality ratios (SMRs) to assess absolute mortality rates. With the exception of a one statistically significant association with duration of exposure to CD and all cancers combined in plant M, we observed no evidence of a positive association with all cancers, RSC or liver cancer and exposure to CD and/or VC using both the unlagged and lagged exposure measures: duration, average intensity or cumulative exposure to CD or VC; time since first CD or VC exposure; and duration of CD exposure or time since first CD exposure in presence or absence of VC exposure. We observed elevated and statistically significantly elevated RRs for some analysis subgroups, but these were due to inordinately low death rates in the baseline categories. With the possible exception of all cancer mortality in plant G, our additional adjustment of RRs for pay type revealed no evidence of positive confounding by smoking. We conclude that exposures to CD or VC at the levels encountered in the four study sites do not elevate mortality risks from all cancers, RSC or liver cancer. This conclusion is corroborated by our analysis of general mortality patterns among the CD cohort reported in our companion paper [G. Marsh, A. Youk, J. Buchanich, M. Cunningham, N. Esmen, T. Hall, M. Phillips, Mortality patterns among industrial workers exposed to chloroprene and other substances. I. General mortality patterns, Chem.-Biol. Interact., submitted for publication].

Chemical Industry↗
PubMed2006

Employment as a welder and Parkinson disease among heavy equipment manufacturing workers.

OBJECTIVE: We investigated whether employment as a welder with potential exposure to manganese and other substances is associated with Parkinson disease (PD), parkinsonism or related neurological disorders, or accelerates the age of onset of PD. METHODS: We selected cases and controls from 12,595 persons ever employed at three Caterpillar Inc. (CAT) plants between 1976 and 2004 with potential to make a medical insurance claim between 1998 and 2004. Cases had filed a claim for 1) PD, 2) "secondary parkinsonism", 3) "other degenerative diseases of the basal ganglia" or 4) "essential and other specific forms of tremor". Cases were grouped by claims: Group 1-claims 1 and 2 and Group 2-claims 1 to 4, and as study period incident (SPI) or prevalent. Each case was matched to two series of 10 controls each on date of case's first claim, year of birth, race and sex. Series I was also matched on plant. RESULTS: Odds ratios (OR) and 95% confidence intervals (CI) for the variable, "ever welder in any CAT plant" were: Group 1-SPI Cases: Series I (OR = .76, CI = .26-2.19), Series II (OR = .81, CI = .29-2.25); Group 1- Prevalent Cases: Series I (OR = .82, CI = .36-1.86), Series II (OR = .97, CI = .42-2.23); Group 2- SPI Cases: Series I (OR = 1.03, CI = .57-1.87), Series II (OR = 1.21, CI = .67-2.20) Group 2-Prevalent Cases: Series I (OR = 1.02, CI = .62-1.71), Series II (OR = .86, CI = .51-1.43). Our finding of no statistically significant associations for welding employment was maintained following adjustment for potential confounding and evaluation of possible effect modification. Employment as a welder did not accelerate the age of onset of PD. CONCLUSIONS: Our study supported the conclusion that employment as a welder is not associated with Parkinson disease, parkinsonism or a related neurological disorder.

Adult↗
PubMed2005

Underascertainment of deaths using social security records: a recommended solution to a little-known problem.

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.

Cohort Studies↗
PubMed2005

Mortality patterns among workers in a US pharmaceutical production plant.

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.

Adult↗
PubMed2005

Reevaluation of mortality risks from nasopharyngeal cancer in the formaldehyde cohort study of the National Cancer Institute.

OBJECTIVE: To determine whether the National Cancer Institute's (NCI) recent suggestion of a causal association between formaldehyde exposure and mortality from nasopharyngeal cancer (NPC) is robust with respect to alternative methods of data analysis and alternative categorizations of formaldehyde exposure. METHODS: The original authors provided the cohort data. We computed U.S. and local county (regional) 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, cumulative, and duration of exposure), using both NCI categories and an alternative categorization based on tertiles of all NPC deaths among exposed subjects. We computed SMRs and RRs for each of 10 study plants and by plant group (Plant 1 (n = 4261) vs. Plants 2-10 (n = 21,358)). RESULTS: Six of 10 NPC deaths observed in the NCI study occurred in only one plant (Plant 1) and the remaining four cases occurred individually in four of the other nine plants studied. A large, statistically significant, regional rate-based NPC SMR of 10.32 (95% CI = 3.79-22.47) among formaldehyde-exposed workers in Plant 1 contrasted sharply with a 35% deficit in NPC deaths (SMR = .65, 95% CI = .08-2.33) among exposed workers in Plants 2-10 combined. The statistically significant exposure-response relationship with formaldehyde and NPC reported in the NCI study for highest peak exposure was driven entirely by a large, statistically significant excess NPC risk in Plant 1 for the highest peak exposure category (4+ ppm). For the remaining nine plants, RRs for all non-baseline highest peak exposure categories were less than 1.0, and we observed no evidence of an exposure-response relationship. Most of the observed NPC excesses for the non-baseline categories of the other exposure metrics (average intensity, cumulative, and duration of formaldehyde exposure) were concentrated in Plant 1, and by contrast to the NCI findings, none of the corresponding exposure-response relationships was statistically significant. CONCLUSIONS: Overall, our reanalysis provided little evidence to support NCI's suggestion of a causal association between formaldehyde exposure and mortality from NPC. NCI's conclusion of a possible causal association was driven heavily by anomalous findings in one study plant (Plant 1). An independent and larger study of Plant 1 by the current authors concluded the NPC excess was not associated with formaldehyde exposure. Our findings cast considerable additional uncertainty regarding the validity of NCI's suggested causal association.

Academies and Institutes↗
PubMed2005

Asthma home teaching: two evaluation approaches.

The aim of this research was to measure the impact of home-based teaching on reducing asthma admissions and emergency department (ED) visits for Medicaid-managed care patients utilizing two different study design methods. This was an historical-prospective study utilizing health plan administrative data, including membership files and medical claims. We identified 381 patients aged 2-56 with hospitalizations or ED visits for asthma. These high risk asthma members were recruited for a home-based teaching program to prevent future hospitalizations or ED visits. We evaluated program effectiveness using two quasi-experimental research designs: a "one-group pre/post-test design," where enrolled members served as their own control, and a more rigorous "untreated control group design with pre/post test," where results for enrolled members and a similar control group were compared pre/post test. Poisson regression models were used to investigate the dependence of member rates for asthma-related events on program enrollment, age, sex, race, and geographic region. Using the pre/post test design, members enrolled in the home-based teaching program demonstrated statistically significant reductions in hospital admissions and ED visits (p < 0.001). The untreated control group design, however, found no association between utilization and enrollment in the home-based teaching program (p = 0.510). Small differences were detected for subgroups. A marginally statistically significant impact of the program was found for Whites, but not for Blacks. The quasi-experimental design that utilized an external control group provided an approach that more accurately explained true disease management program impact. In addition, this approach allowed for subgroup analyses to detect opportunities for program improvement.

Adolescent↗
PubMed2004

A method for imputing missing data in longitudinal studies.

PURPOSE: In a cohort in which racial data are unknown for some persons, race-specific persons and person-years are imputed using a model-based iterative allocation algorithm (IAA). METHODS: An EM algorithm-based approach to address misclassification in a censored data regression setting can be adapted to estimate the probability that a person of unknown race is white. The corresponding race-specific person-years are obtained as a by-product of the estimation procedure. Variance estimates are computed using the bootstrap. The proposed approach is compared with the proportional allocation method (PAM). RESULTS: In an occupational cohort where racial data were missing for 41% of the workers, the age-time-race-specific person-years were estimated within a relative variation of approximately 20%, using the IAA. The deaths were less reliably estimated. The standardized mortality ratios (SMRs) for all-cause mortality estimated using the IAA and the PAM were more similar for the non-white workers than for a smaller subgroup of white workers. CONCLUSIONS: The IAA provides a method to reliably estimate race-specific person-year denominators in cohort studies with missing racial data. This method is applicable to other incompletely observed non-time-dependent categorical covariates. Internal cohort rates or SMRs can be computed and modeled, with bootstrap confidence intervals that account for the uncertainty in the determination of race.

Adolescent↗
PubMed2004

Reevaluation of mortality risks from leukemia in the formaldehyde cohort study of the National Cancer Institute.

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.

Cohort Studies↗
PubMed2004

Historical cohort study of U.S. man-made vitreous fiber production workers IX: summary of 1992 mortality follow up and analysis of respiratory system cancer among female workers.

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.

Adult↗
PubMed2004

A 50-year historical cohort mortality study of workers in a pharmaceutical plant.

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.

Cause of Death↗
PubMed2004

A risk assessment for occupational acrylonitrile exposure using epidemiology data.

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.

Acrylonitrile↗
PubMed2003

The Drake Health Registry Study: findings from fifteen years of continuous bladder cancer screening.

BACKGROUND: The Drake Health Registry Study (DHRS) is an ongoing bladder cancer screening program initiated in 1986 due to workers' probable past exposure to the bladder carcinogen, beta-naphthylamine (BNA). METHODS: At periodic screening visits, a health survey is administered and three screening tests are applied to a urine sample, urinalysis (UA), papanicolaou (PAP), and quantitative fluorescence image analysis (QFIA). Positive screens are eligible for a free bladder cystoscopy with random biopsies. RESULTS: Forty of 51 persons eligible for diagnostic evaluation underwent cystoscopy. One person was diagnosed with carcinoma in situ, two with transitional cell papilloma, 14 with dysplasia, two of which developed transitional cell carcinoma; 26 had bladder abnormalities such as chronic inflammation, chronic cystitis, atypical changes, atypia, hyperplasia, or papillary clusters. CONCLUSIONS: The DHRS continues to identify early stage bladder cancer and other abnormalities among workers exposed to BNA before 1981 and generates useful clinical, psycho-social, and epidemiologic data.

2-Naphthylamine↗