Exposure to benzene in a pooled analysis of petroleum industry case-control studies.

Cases of lymphohematopoietic cancer from three petroleum industry cohorts, matched to controls from the respective cohort, were pooled into single study. Average benzene exposure was quantitatively estimated in ppm for each job based on measured data from the relevant country, adjusted for the specific time period, site and job exposure characteristics and the certainty of the exposure estimate scored. The probability of dermal exposure and of peak exposure was also assessed. Before risk was examined, an exposure estimate comparison and rationalisation exercise was performed across the studies to ensure accuracy and consistency of approach. This article evaluates the final exposure estimates and their use in the risk assessments. Overall benzene exposure estimates were low: 90% of participants accumulated less than 20 ppm-years. Mean cumulative exposure was estimated as 5.15 ppm-years, mean duration was 22 years, and mean exposure intensity was 0.2 ppm. 46% of participants were allocated a peak exposure (>3 ppm at least weekly). 40% of participants had a high probability of dermal exposure (based on the relative probability of at least weekly exposure). There were differences in mean intensity of exposure, probability of peak, and/or dermal exposure associated with job category, job site, and decade of exposure. Terminal Operators handling benzene-containing products were the most highly exposed group, followed by Tanker Drivers carrying gasoline. Exposures were higher around 1940-1950 and lower in more recent decades. Overall confidence in the exposure estimates was highest for recently held jobs and for white-collar jobs. We used sensitivity analyses, which included and excluded case-sets on the basis of exposure certainty scores, to inform the risk assessment. The above analyses demonstrated that the different patterns of exposure across the three studies are largely attributable to differences in jobs, site types, and time frames rather than study. This provides reassurance that the previous rationalisation of exposures achieved inter-study consistency and that the data could be confidently pooled.

Acute myeloid and chronic lymphoid leukaemias and exposure to low-level benzene among petroleum workers.

BACKGROUND: High benzene exposure causes acute myeloid leukaemia (AML). Three petroleum case-control studies identified 60 cases (241 matched controls) for AML and 80 cases (345 matched controls) for chronic lymphoid leukaemia (CLL). METHODS: Cases were classified and scored regarding uncertainty by two haematologists using available diagnostic information. Blinded quantitative benzene exposure assessment used work histories and exposure measurements adjusted for era-specific circumstances. Statistical analyses included conditional logistic regression and penalised smoothing splines. RESULTS: Benzene exposures were much lower than previous studies. Categorical analyses showed increased ORs for AML with several exposure metrics, although patterns were unclear; neither continuous exposure metrics nor spline analyses gave increased risks. ORs were highest in terminal workers, particularly for Tanker Drivers. No relationship was found between benzene exposure and risk of CLL, although the Australian study showed increased risks in refinery workers. CONCLUSION: Overall, this study does not persuasively demonstrate a risk between benzene and AML. A previously reported strong relationship between myelodysplastic syndrome (MDS) (potentially previously reported as AML) at our study's low benzene levels suggests that MDS may be the more relevant health risk for lower exposure. Higher CLL risks in refinery workers may be due to more diverse exposures than benzene alone.

Influence of toluene co-exposure on the metabolism and genotoxicity of benzene in mice using continuous and intermittent exposures.

Benzene exposure in occupational settings often occurs with concurrent exposure to toluene, the methyl-substituted derivative of benzene. Toluene is also readily metabolized by CYP450 isozymes although oxidation primarily occurs in the methyl group. While earlier mouse studies addressing co-exposure to benzene and toluene at high concentrations demonstrated a reduction in benzene-induced genotoxicity, we have previously found, using an intermittent exposure regimen with lower concentrations of benzene (50 ppm) and toluene (100 ppm), that toluene enhances benzene-induced clastogenic or aneugenic bone marrow injury in male CD-1 mice with significantly increased CYP2E1, and depleted GSH and GSSG levels. The follow-up study reported here also used the same daily and total co-exposures but over consecutive days and compared the effects of co-exposure on genotoxicity and metabolism in CD-1 mice both with and without buthionine sulfoximine (BSO) treatment to deplete GSH. In this study the toluene co-exposure doubled the genotoxic response (as determined by the erythrocyte micronucleus test) to benzene alone. Further, GSH depletion caused a reduction in this genotoxicity in both benzene exposed and benzene/toluene co-exposed mice. The results are discussed in terms of the analyses of urinary metabolites from this consecutive day study and the intermittent exposure study as well as levels of CYP2E1, epoxide hydrolase, quinone reductase, alcohol dehydrogenase, and aldehyde dehydrogenase activities. The results suggest that the presence of glutathione is necessary for benzene genotoxicity either as a metabolite conjugate or through an indirect mechanism such as TNF-induced apoptosis.

Ensuring comparability of benzene exposure estimates across three nested case-control studies in the petroleum industry in support of a pooled epidemiological analysis.

BACKGROUND: Three case-control studies each nested within a cohort of petroleum workers assessed exposure to benzene in relation to risk of haematopoietic cancers. These studies have each been updated and the cases will be pooled to derive a more powerful study. The benzene exposure of new leukemia cases and controls was estimated in accordance with each respective study's original methods. An essential component of the process of pooling the data was comparison and rationalisation of the exposure estimates to ensure accuracy and consistency of approach. This paper describes this process and presents comparative estimates before and after appropriate revision took place. The original petroleum industry studies, in Canada, the UK and Australia, were conducted at different points in time by different study teams, but the industry used similar technology in similar eras in each of these countries. METHODS: A job history for each subject giving job title, dates of starting and leaving the job and location of work, was assembled. For each job or task, the average benzene exposure (Base Estimate (BE) in ppm) was derived from measurements collected at applicable worksites. Estimates of exposure intensity (workplace exposure estimates (WE)) were then calculated for each line of work history by adjusting the BEs for site- and era-specific exposure-related variables such as loading technology and percentage benzene in the product. To ensure that the exposure estimates were comparable among the studies, the WEs were allocated to generic Job Categories, e.g. Tanker Driver (by technology used e.g. bottom loading), Motor Mechanic. The WEs were stratified into eras, reflecting technological changes in the industry. The arithmetic mean (AM), geometric mean (GM) and range of the stratified WEs were calculated, by study, for each generic Job Category. These were then compared. The AMs of the WEs were regarded as substantially similar if they were within 20% in all three studies in one era or for at least two studies in two eras. If the AM of the WE group differed by more than 20%, the data were examined to see whether the difference was justified by differences in local exposure conditions, such as an enclosure versus open work area. Estimates were adjusted in the absence of justification for the difference. RESULTS: Reconciliation of differences resulted in changes to a small number of underlying BEs, particularly the background values, also the BEs attributed to some individuals and changes to the allocation of jobs between Job Categories. Although the studies covered some differing sectors of the industry and different time periods, for 22 Job Categories there was sufficient overlap, particularly in the downstream distribution sector, to make comparisons possible. After adjustment 12 Job Categories were judged to be similar and 10 were judged to be justifiably different. Job-based peak and skin exposure estimates were applied in a uniform way across the studies and a single approach to scoring the certainty of the exposure estimates was identified. CONCLUSIONS: The revised exposure estimates will be used in the pooled analysis to examine the risk of haematopoietic cancers and benzene exposure. This exercise provided an important quality control check on the exposure estimates and identified similarly exposed Job Categories that could be grouped for risk assessment analyses.

Analysis of hydroquinone and catechol in peripheral blood of benzene-exposed workers.

We have developed a gas chromatography-mass spectrometry method for analysis of benzene (BZ) metabolites in human urine and blood. Here we describe peripheral blood concentrations of hydroquinone (HQ(1)) and catechol (CAT(2)) in total, protein-bound, and unbound (free) forms obtained from BZ-exposed factory workers and controls. Total and unbound metabolites were directly measured in independent experiments, while bound forms were calculated as [total]-[unbound]. In this subset of a larger study, breathing zone benzene, toluene, and xylene were measured for the duration of a workshift, and end-shift blood samples taken from 143 subjects and controls. Potential lifestyle and environmental influences were assessed by questionnaire and bioassay, and single nucleotide polymorphisms in xenobiotic metabolizing enzymes NQO1, MPO, CYP2E1, and GSTT1 were also analyzed for potential contribution to differences in blood metabolite concentration. Total CAT, bound CAT, total HQ, and bound HQ correlated well with benzene exposure, while unbound CAT and HQ displayed no correlation. Nearly all of the metabolites found in blood were bound to protein (CAT 96-99+%, HQ 78-92+%), and when the ratio of bound to unbound metabolites were compared in subsets of exposed workers, the increase in blood metabolite concentration was nearly all due to an increase in the protein-bound molecule. These findings suggest that a threshold for conjugation does not exist within the exposure spectrum studied (0.01-78.8 mg/m(3)). This method demonstrates the feasibility of analyzing benzene metabolites in human blood, and should allow for further investigation of the health effects of benzene and its metabolites.

Benzene exposure in industries using or manufacturing paint in China--a literature review, 1956-2005.

A systematic review of the Chinese literature was conducted from 1956 to 2005. The survey included both online and manual searching, as well as expert discussions aimed at providing insight into factors affecting benzene exposure levels in paint/coatings industries. Data extracted from 204 papers included: (1) year of occurrence, (2) type of paint/coatings products, (3) type of industries where the products were used or produced, (4) job titles and work activities, (5) type of literature searched, (6) working conditions whenever data were available, and (7) exposure levels. Most benzene measurements were short-term samples for comparison with the Chinese maximum allowable concentration standard. The accuracy and precision of the sampling and analytical methods were not reported. The distribution of benzene concentrations was tested and found to fit neither normal nor lognormal distributions. Analysis of variance (comparison for more than two groups) and t-test (comparison for two groups) were conducted on Blom-transformed benzene concentration data. The overall median benzene exposure levels were 215, 82, 31, and 6 mg/m(3) during the periods 1956-1978, 1979-1989, 1990-2001, and 2002-2005, respectively. Mean benzene exposure was significantly lower for paint manufacturing than paint spraying. No significant difference was found among paint types and benzene exposure for paint application. Benzene exposure was significantly higher in workplaces judged to have poor ventilation. No significant differences were found in benzene exposure as a function of industry type. Even though substantially lower when compared with levels in the past, recent benzene exposure measurements suggested that many facilities in the paint/coatings industries in China still have benzene concentrations that are above the current China occupational exposure limit for benzene (6 mg/m(3) as a time-weighted average). Benzene concentrations from the present exercise, while not directly supporting quantitative retrospective exposure estimating, provide insight on relative benzene exposure for painting tasks in the reported industries over time.

Mortality and cancer morbidity in a cohort of Canadian petroleum workers.

AIMS: To assess mortality and cancer morbidity in Canadian petroleum workers and explore exposure-response relations for specific petroleum agents. METHODS: A total of 25 292 employees hired between 1964 and 1994 were linked to the Canadian tumour registry and national mortality database. Exposure-response trends were assessed for hydrocarbon solvents/fuels, hydrocarbon lubricants, petroleum coke/spent catalyst, and hydrogen sulphide (H2S). RESULTS: External comparison analyses (mortality and incidence) showed deficits for all causes and all malignant neoplasms combined and were consistent with expectation for most malignant and non-malignant sites analysed. Gall bladder cancer mortality was increased among males based on four deaths, but cases had no common job assignments and the increase was focused in workers employed <10 years. Mesothelioma incidence was increased. Most exposure-specific analyses were compromised by small numbers. Statistically significant increases were observed for H2S exposure and a subgroup of accidental deaths as well as for petroleum coke/spent catalyst exposure and lung cancer. While both findings have a degree of biologic plausibility, the H2S association, which exhibited a clearer exposure-response pattern, could be subject to unmeasured confounders. Additionally, interpretation was complicated by the high correlation between hydrocarbon and H2S exposures. With regard to lung cancer, the analysis could not adequately control for smoking, was based on small numbers, and exhibited a tenuous exposure-response pattern. CONCLUSION: The findings for mesothelioma suggest the need for continued attention to asbestos in the petroleum industry. The relation between accidental deaths and H2S exposure deserves closer scrutiny in similarly exposed populations. Further analyses of lung cancer are underway and will be reported separately.

Using epidemiological studies to check the consistency of the cancer risks predicted by high-dose animal experiments: a methodological review.

Epidemiological studies have been cited in the literature as evidence both for and against the human cancer risks predicted by high-exposure rodent studies. However, there has been little overall consistency in the ways that these animal-to-human comparisons have been made. This review examines some examples of these types of comparisons and describes the methods and techniques used by different investigators. Eleven "key decision areas" that need to be addressed are identified and recommendations for consistent, logical, and statistically appropriate approaches that might be taken to standardize the process are provided. In general, it is suggested that investigators provide the most useful information when they use logical, transparent, and statistically valid comparisons to pursue limited and focused objectives, such as directly testing the validity of an existing regulatory guidance value. Other recommendations include selecting biologically plausible extrapolative models that fit the data and drawing conclusions that are consistent with the study results and objectives.

Updated mortality among diverse operating segments of a petroleum company.

OBJECTIVES: To update mortality for 34 560 employees from diverse operating segments of a Canadian petroleum company; and to investigate potential relations with occupational factors. METHODS: Employees from 1964-83 were linked to the Canadian mortality data base to provide 11 years additional follow up. There were 6760 deaths and 750 683 person-years of follow up compared with 3909 and 428 190, respectively, in the earlier study. Analyses used standardised mortality ratios (SMRs) to compare worker cause specific mortality with the Canadian general population. Duration of employment and latency analyses were performed for causes previously found to be increased in this and other petroleum cohorts, as well as any findings of interest. RESULTS: For the period 1964-94, employees experienced significantly low overall mortality (SMR=0.86 men, SMR=0.80 women). Kidney cancer, which has been increased in some studies of petroleum workers, was not increased. Acute non-lymphocytic leukaemia in exposed operating segments was consistent with the expected or only slightly, non-significantly increased. The most notable finding was increased deaths from mesothelioma among refinery and petrochemical workers (SMR 8.68; 95% confidence interval (95% CI) 5.51 to 13.03), most of whom were long term employees in jobs with presumed exposure to asbestos (mechanical and pipefitters). Deaths from multiple myeloma among marketing and distribution workers, which were previously increased, remained increased (SMR 2.08; 95% CI 0.95 to 3.95) in the update period 1984-94; however, there was no clear pattern by duration of employment or latency. Aortic aneurysms, which also were previously significantly increased among marketing and distribution workers approached the expected in the update period (SMR 1.18; 95% CI 0. 65-1.98). Analyses by duration of employment showed suggestive trends for aortic aneurysms, but earlier studies of this cohort have not found a relation between aortic aneurysms and exposure to hydrocarbons. CONCLUSION: The additional 2851 deaths and 322 493 person-years of follow up strengthened the assessment of mortality patterns relative to occupational factors. With the exception of mesothelioma, no clear work related increases in disease were identified.

Influence of parental and biological factors on the male birth fraction in the United States: an analysis of birth certificate data from 1964 through 1988.

OBJECTIVE: To determine the role of parental and biological factors on the U.S. male birth fraction from 1964 through 1988. DESIGN: Logistic regression on annual U.S. male births by race group. SETTING: Population-based data. PATIENT(S): Live births in the United States 1964 through 1988. INTERVENTION(S): None. MAIN OUTCOME MEASURE(S): Annual U.S. male birth fraction by parental and biological factors. RESULT(S): During the study period, the annual U. S. male birth fraction showed changes based on race group, parental age, and low birth weight. The overall influence of parental age on the U.S. male birth fraction is strong and is stronger in nonwhites than in whites. The U.S. male birth fraction is also strongly influenced by the percentage of low birth weight infants in nonwhites, but not in whites. The male birth fraction declines with increasing age of either parent and with an increase in the percentage of low birth weight infants. CONCLUSION(S): The relative magnitude of influences on the U.S. male birth fraction depend on the race group, which may be a reflection of the range of observed data rather than biological differences. The developed models have reasonable predictive power and are an appropriate first step in understanding the factors influencing the male birth fraction. These types of parental and biological variables should be included in models before examining other exogenous and population level variables.

A framework for addressing health issues in or near a manufacturing facility.

Clustering of health events in or around industrial facilities sometimes leads to worker and community concerns that plant management or local health professionals must address. We provide an eight-step process to deal with these concerns systematically. We emphasize the use of good scientific practices with managerial oversight for effective worker and community communication. This process is directed to plant management and the local health professional and emphasizes the practical aspects of the investigation.

Quantifying uncertainty in a risk assessment using human data.

A call for risk assessment approaches that better characterize and quantify uncertainty has been made by the scientific and regulatory community. This paper responds to that call by demonstrating a distributional approach that draws upon human data to derive potency estimates and to identify and quantify important sources of uncertainty. The approach is rooted in the science of decision analysis and employs an influence diagram, a decision tree, probabilistic weights, and a distribution of point estimates of carcinogenic potency. Its results estimate the likelihood of different carcinogenic risks (potencies) for a chemical under a specific scenario. For this exercise, human data on formaldehyde were employed to demonstrate the approach. Sensitivity analyses were performed to determine the relative impact of specific levels and alternatives on the potency distribution. The resulting potency estimates are compared with the results of an exercise using animal data on formaldehyde. The paper demonstrates that distributional risk assessment is readily adapted to situations in which epidemiologic data serve as the basis for potency estimates. Strengths and weaknesses of the distributional approach are discussed. Areas for further application and research are recommended.

Mortality experience of a young petrochemical industry cohort. 1979-1992 follow-up study of US-based employees.

This retrospective study examines the mortality patterns of a relatively young cohort of 81,746 former and current petrochemical company employees. Standardized mortality ratios (SMR) for 1979 through 1992 are generally from about unity to well below unity for major causes and numerous specific causes of death studied by gender/race/job subgroups. Findings of note include a SMR (based on incidence rates) of 1.94 (95% confidence interval [CI], 1.04 to 3.33) for mesothelioma, and a SMR of 1.81 (95% CI, 0.90 to 3.24) for chronic lymphocytic leukemia, both among males hired before 1960. All male semiskilled operatives have a 1.6-fold increase (95% CI, 1.07 to 2.29) in motor vehicle accident deaths, with declining rates since the mid-1980s. The overall SMR for acquired immunodeficiency syndrome (AIDS) is at unity (69 deaths), with excesses in technician and office worker subgroups. Four decedents with lymphoma (code 202.8 in 9th revision ICD) had AIDS as a secondary cause of death, suggesting the need to examine secondary causes when studying lymphopoietic conditions. This routine surveillance activity provides leads regarding the presence or absence of excess mortality risk.

Determination of leukemogenic benzene exposure concentrations: refined analyses of the Pliofilm cohort.

Biologic data on benzene metabolite doses, cytotoxicity, and genotoxicity often show that these effects do not vary directly with cumulative benzene exposure (i.e., concentration times time, or c x t). To examine the effect of an alternate exposure metric, we analyzed cell-type specific leukemia mortality in Pliofilm workers. The work history of each Pliofilm worker was used to define each worker's maximally exposed job/department combination over time and the associated long-term average concentration associated with the maximally exposed job (LTA-MEJ). Using this measure, in conjunction with four job exposure estimates, we calculated SMRs for groups of workers with increasing LTA-MEJs. The analyses suggest that a critical concentration of benzene exposure must be reached in order for the risk of leukemia or, more specifically, AMML to be expressed. The minimum concentration is between 20 and 60 ppm depending on the exposure estimate and endpoint (all leukemias or AMMLs only). We believe these analyses are a useful adjunct to previous analyses of the Pliofilm data. They suggests that (a) AMML risk is shown only above a critical concentration of benzene exposure, measured as a long-term average and experienced for years, (b) the critical concentration is between 50 and 60 ppm when using a median exposure estimate derived from three previous exposure assessments, and is between 20 and 25 ppm using the lowest exposure estimates, and (c) risks for total leukemia are driven by risks for AMML, suggesting that AMML is the cell type related to benzene exposure.

The relationship between low-level benzene exposure and leukemia in Canadian petroleum distribution workers.

This study was conducted to evaluate the relationship between leukemia occurrence and long-term, low-level benzene exposures in petroleum distribution workers. Fourteen cases were identified among a previously studied cohort [Schnatter et al., Environ Health Perspect 101 (Suppl 6):85-89 (1993)]. Four controls per case were selected from the same cohort, controlling for birth year and time at risk. Industrial hygienists estimated workplace exposures for benzene, without knowledge of case-control status. Average benzene concentrations ranged from 0.01 to 6.2 ppm. Company medical records were used to abstract information on other potential confounders such as cigarette smoking. Odds ratios were calculated for several exposure metrics. Conditional logistic regression modeling was used to control for potential confounders. The risk of leukemia was not associated with increasing cumulative exposure to benzene for these exposure levels. Duration of benzene exposure was more closely associated with leukemia risk than other exposure metrics, although results were not statistically significant. A family history of cancer and cigarette smoking were the two strongest risk factors for leukemia, with cumulative benzene exposure showing no additional risk when considered in the same models. This study is consistent with other data in that it was unable to demonstrate a relationship between leukemia and long-term, low-level benzene exposures. The power of the study was limited. Thus, further study on benzene exposures in this concentration range are warranted.

Lymphohaematopoietic malignancies and quantitative estimates of exposure to benzene in Canadian petroleum distribution workers.

OBJECTIVE: To evaluate the relation between mortality from lymphohaematopoietic cancer and long term, low level exposures to benzene among male petroleum distribution workers. METHODS: This nested case control study identified all fatal cases of lymphohaematopoietic cancer among a previously studied cohort. Of the 29 cases, 14 had leukaemia, seven multiple myeloma, and eight non-Hodgkin's lymphoma. A four to one matching ratio was used to select a stratified sample of controls from the same cohort, controlling for year of birth and time at risk. Industrial hygienists estimated workplace exposures for benzene and total hydrocarbons, without knowledge of case or control status, for combinations of job, location, and era represented in all work histories. Average daily benzene concentrations ranged from 0.01 to 6.2 parts per million (ppm) for all jobs. Company medical records were used to abstract information on other potential confounders such as cigarette smoking, although the data were incomplete. Odds ratios (ORs) were calculated with conditional logistic regression techniques for several exposure variables. RESULTS: Risks of leukaemia, non-Hodgkin's lymphoma, and multiple myeloma were not associated with increasing cumulative exposure to benzene or total hydrocarbons. For leukaemia, the logistic regression model predicted an OR of 1.002 (P < 0.77) for each ppm-y of exposure to benzene. Duration of exposure to benzene was more closely associated with risk of leukaemia than other exposure variables. It was not possible to completely control for other risk factors, although there was suggestive evidence that smoking and a family history of cancer may have played a part in the risk of leukaemia. CONCLUSION: This study did not show a relation between lymphohaematopoietic cancer and long term, low level exposures to benzene. The power of the study to detect low-such as twofold-risks was limited. Thus, further study on exposures to benzene in this concentration range are warranted.

Retrospective benzene and total hydrocarbon exposure assessment for a petroleum marketing and distribution worker epidemiology study.

A quantitative exposure-estimating algorithm for benzene and total hydrocarbons was developed for a case control study of petroleum marketing and distribution workers. The algorithm used a multiplicative model to adjust recently measured quantitative exposure data to past scenarios for which representative exposure measurement data did not exist. This was accomplished through the development of exposure modifiers to account for differences in the workplace, the materials handled, the environmental conditions, and the tasks performed. Values for exposure modifiers were obtained empirically and through physical/chemical relationships. Dates for changes that altered exposure potential were obtained from archive records, retired employee interviews, and from current operations personnel. Exposure modifiers were used multiplicatively, adjusting available measured data to represent the relevant exposure scenario and time period. Changes in exposure modifiers translated to step changes in exposure estimates. Though limited by availability of data, a validation exercise suggested that the algorithm provided accurate exposure estimates for benzene (compared with measured data in industrial hygiene survey reports); the estimates generally differed by an average of less than 20% from the measured values. This approach is proposed to quantify exposures retrospectively where there are sufficient data to develop reliable current era estimates and where a historical accounting of key exposure modifiers can be developed, but where there are insufficient historic exposure measurements to directly assess historic exposures.

Colorectal cancer incidence among polypropylene manufacturing workers. An update.

This study updates an earlier investigation that found a sixfold excess incidence of colorectal cancer among polypropylene workers for the period January 1960 to September 1985. The study cohort comprised 412 male workers with at least 6 months employment and 10 years latency. For the extended follow-up period (October 1985 to May 1992), the standardized incidence ratio (SIR) based on state comparison rates was slightly elevated and not statistically significant (SIR = 1.5, 95% confidence interval [CI] = 0.5 to 3.5). A 2.3-fold excess was observed among process workers (95% CI = 0.3 to 8.2), but this was based on only two cases. Risk among process/mechanical workers was greater for short-term workers (< 10 years, SIR = 3.2, 95% CI = 0.7 to 9.2) compared with longer-term workers (> or = 10 years, SIR = 0.7, 95% CI = 0.02 to 4.0). Overall, the update findings do not suggest an occupationally related risk. Possible influences of company-sponsored colorectal cancer screening, the polyolefin unit shutdown, and other factors are discussed.

Colorectal polyp incidence among polypropylene manufacturing workers.

To follow up earlier findings of increased colorectal cancer and polyp risk among a group of Texas polypropylene manufacturing workers, a second company-sponsored colorectal cancer screening program was conducted. Ninety-four (64%) of the 147 male workers negative for polyps in the first screening were rescreened. Age- and examiner-adjusted incidence rate ratios (IRRs) were modestly elevated for polypropylene manufacturing workers compared with patients screened at the same clinic for total (IRR = 1.31; 90% confidence interval [CI] = 0.84 to 2.03) and adenomatous (IRR = 1.80; 90% CI = 0.68 to 4.78) polyps. However, risk of adenomas among the highest exposed group (early term process/mechanical workers: IRR = 1.77; 90% CI = 0.51 to 6.18) was similar to risk in the least-exposed group (engineer/chemist/administrative workers: IRR = 2.02; 90% CI = 0.56 to 7.31). The modest, nonsignificant excesses and the similarity in risk across job categories does not suggest an occupationally related risk, although small numbers and potential biases preclude making definitive conclusions.

A retrospective mortality study among Canadian petroleum marketing and distribution workers.

We conducted a retrospective mortality study among 6672 petroleum marketing and distribution workers from 226 locations throughout Canada. These employees worked for at least 1 year in the marketing distribution segment from 1964 through 1983 or were annuitants as of 1964. Industrial hygienists assigned hydrocarbon (HC) exposure frequency scores for several jobs, departments, and job functions. We computed standardized mortality ratios for the total cohort, HC exposure frequency groups, and tank truck drivers, and we also used Poisson regression techniques to model mortality for selected causes of death according to HC exposure frequency. Results indicate overall mortality below that of the general Canadian population for all marketing distribution workers [Standardized mortality ratio (SMR) = 0.88]. Mortality from aortic aneurysms was significantly elevated in all marketing/distribution workers (SMR = 1.79) but was due to raised mortality in nonexposed workers (SMR = 2.80). Tank truck drivers showed significantly elevated mortality due to leukemia (SMR = 3.35) based on five deaths. The leukemia findings were not evident in the larger group of marketing distribution workers classified as exposed to hydrocarbons (SMR = 1.01). No other cause of death was elevated in truck drivers. The leukemia findings are suggestive of a possible influence due to exposure to HCs in tank truck drivers, although other explanations cannot be ruled out. Other findings of elevated mortality in the marketing distribution group are generally not statistically significant. These included moderately increased mortality due to multiple myeloma, malignant melanoma, and kidney cancer. Small numbers of observed and expected deaths limit concise interpretations for these diseases.