Lymphohematopoietic Cancers Research Articles

Mortality and cancer incidence in New Zealand meat workers

Aims: To ascertain whether there is an increased risk of cancers of the lung and lymphohaematopoietic tissue in workers employed in the New Zealand meat processing industry, and to identify...

Dietary Fish Intake and Risk of Leukaemia, Multiple Myeloma, and Non-Hodgkin Lymphoma

Abstract This study aimed to determine whether fish intake was protective against leukemia, multiple myeloma, and non-Hodgkin lymphoma (NHL), and if our previous finding of a protective effect of fish-related occupations on the risk of these diseases was due to dietary intake of fish. We used data from a population-based case-control study undertaken in Canada in 1994–1998. Dietary information was available for 919 leukemia cases, 287 myeloma cases, 1418 NHL cases, and 4202 controls. The risk of each of the three cancers was determined using multiple logistic regression analysis according to quartiles of weekly fresh fish intake, percentage of total energy intake from fresh fish, and percentage of total fat intake from fresh fish. After adjusting for age, sex, smoking, BMI, and proxy status, people who consumed greater proportions of their total energy intake from fresh fish had a significantly lower risk of each of the three types of cancer, and there was a significant dose-response for risk of leukemia and NHL. Those in the highest quartile for percentage of fat intake from fish were at lowest risk: leukemia odds ratio (OR) 0.72, 95% confidence interval (CI) 0.58–0.89; multiple myeloma OR 0.64, 95% CI 0.45–0.90; NHL OR 0.71, 95% CI 0.60–0.85; and all LH cancers combined OR 0.70, 95% CI 0.61–0.81. The protective effect previously observed for working with fish on the risk of leukemia and lymphoma was independent of fish intake. These findings suggest that a diet high in fish may be protective against lymphohematopoietic cancers and confirm the reduced risk among fish workers.

Lymphohaematopoietic cancer risk among chemical workers exposed to benzene

Aims: To determine cause specific mortality in a cohort of 2266 chemical workers exposed to benzene in various manufacturing processes after 1935. Methods: The cohort has accumulated over 80 000...

CANCER INCIDENCE AMONG PESTICIDE APPLICATORS EXPOSED TO ALACHLOR OR ATRAZINE IN THE AGRICULTURAL HEALTH STUDY

Objectives We evaluated the cancer incidence among over 49,000 pesticide applicators with exposure to either alachlor or atrazine in the Agricultural Health Study (AHS), a prospective cohort study of over 89,000 restricted use pesticide applicators and spouses of farmer applicators in Iowa and North Carolina, USA. Methods Comprehensive questionnaire data concerning lifestyle, occupations, personal and family medical history and use of 50 important agricultural pesticides, were collected prior to cancer incidence. Standardized incidence ratios (SIR) were estimated for those exposed and those not exposed to alachlor and for those exposed and those not exposed to atrazine, two important agricultural herbicides. Comparing the cancer experience of pesticide applicators from each state with that expected based on state specific incidence rates. Poisson regression was used to controlling for the effects of potential confounders (including age, sex, smoking, alcohol, education, state of residence, enrollment year, family history of cancer and the 5 [in the case of alachlor] or [10 in the case of atrazine] other pesticides most correlated with either alachlor or atrazine). Results A total of 1,466 incident malignant neoplasms occurred during the study period, 1993–2000. The SIR analysis showed a moderate deficit for all malignant neoplasm combined among both users and non-users of these herbicides. In Poisson regression analysis of alachlor, we found a significant increasing trend for the incidence of all lymphohematopoietic cancer and cumulative alachlor exposure (p for trend = 0.02). Incidence of leukemia and multiple myeloma was markedly increased among applicators in the highest exposure category. Similar analyses for other cancers did not suggest any association. For atrazine, no significant exposure-response trends were observed for any cancers or for all cancers combined, but non-significant positive trends were observed for cumulative atrazine exposures cancers of the rectum, bladder, and testicles. Conclusion Our findings suggests an association between alachlor exposure and increased incidence of lymphohematopoietic cancer in the Agricultural Health Study. Findings for atrazine are inconclusive at this time. Although the statistical power of the AHS is still low for some cancer evaluations after only 5.3 years of cohort follow-up, the comprehensive prospectively collected data, especially concerning pesticide exposures is an important strength of the study. Further details of the study are provided at our website: www.aghealth.org. Words = 415

Leukemia risk associated with low-level benzene exposure.

Men who were part of an Australian petroleum industry cohort had previously been found to have an excess of lympho-hematopoietic cancer. Occupational benzene exposure is a possible cause of this excess. We conducted a case-control study of lympho-hematopoietic cancer nested within the existing cohort study to examine the role of benzene exposure. Cases identified between 1981 and 1999 (N = 79) were age-matched to 5 control subjects from the cohort. We estimated each subject's benzene exposure using occupational histories, local site-specific information, and an algorithm using Australian petroleum industry monitoring data. Matched analyses showed that the risk of leukemia was increased at cumulative exposures above 2 ppm-years and with intensity of exposure of highest exposed job over 0.8 ppm. Risk increased with higher exposures; for the 13 case-sets with greater than 8 ppm-years cumulative exposure, the odds ratio was 11.3 (95% confidence interval = 2.85-45.1). The risk of leukemia was not associated with start date or duration of employment. The association with type of workplace was explained by cumulative exposure. There is limited evidence that short-term high exposures carry more risk than the same amount of exposure spread over a longer period. The risks for acute nonlymphocytic leukemia and chronic lymphocytic leukemia were raised for the highest exposed workers. No association was found between non-Hodgkin lymphoma or multiple myeloma and benzene exposure, nor between tobacco or alcohol consumption and any of the cancers. We found an excess risk of leukemia associated with cumulative benzene exposures and benzene exposure intensities that were considerably lower than reported in previous studies. No evidence was found of a threshold cumulative exposure below which there was no risk.

Lymphohaematopoietic system cancer incidence in an urban area near a coke oven plant: an ecological investigation

Aims: To evaluate the incidence risk of lymphohaematopoietic cancers for the 1986–94 period in Cornigliano, a district of Genoa (Italy), where a coke oven is located a few hundred metres...

Animal-related occupations and the risk of leukemia, myeloma, and non-Hodgkin's lymphoma in Canada.

There is some evidence to suggest that workers in animal-related occupations are at increased risk of developing lymphohematopoietic cancers. This study aimed to examine the risk of leukemia, non-Hodgkin's lymphoma (NHL), and multiple myeloma associated with occupational exposure to animals. We used data from a multi-site, population-based case-control study using mailed questionnaires which had taken place in eight of ten Canadian provinces, during 1994-1998. There were 1023 leukemia cases, 1577 NHL cases, and 324 multiple myeloma cases (all histologically confirmed) and 4688 population-based controls. Animal-related occupations were identified from a lifetime occupational history. Subjects in animal-related jobs were compared with others using logistic regression for the risk of leukemia, NHL, and multiple myeloma. Compared to subjects without occupational exposure to animals, occupational exposure to beef cattle increased the risks of leukemia (odds ratio (OR) 2.0, 95% confidence interval (CI) 1.2-3.3) and NHL (OR 1.8, 95% CI 1.1-2.9). No other animal exposure was consistently associated with risk of lymphohematopoietic cancer. An unexpected protective association was observed between work as a fisherman and leukemia (OR 0.4, 95% CI 0.2-0.8) and NHL (OR 0.6, 95% CI 0.4-0.9). This population-based case-control study found that those individuals working in occupations associated with beef cattle are at increased risk for developing leukemia and lymphoma while those working in occupations requiring the handling of fish are at decreased risk of leukemia and lymphoma.

Proportionate mortality among US migrant and seasonal farmworkers in twenty-four states.

US migrant and seasonal farmworkers may be exposed to potentially carcinogenic pesticides and other agents. Little epidemiologic research has been conducted on this population. We examined the proportionate mortality of 26,148 subjects (14,631 white men (WM), 7,299 nonwhite men (NM), 1,081 white women (WW), and 3,137 nonwhite women (NW)) who were identified as farmworkers on death certificates from 24 US states during 1984-1993. Farmworkers had significantly elevated proportionate mortality from injuries, tuberculosis, mental disorders, cerebrovascular disease, respiratory diseases, ulcers, hypertension (NW), and cirrhosis (NW). There was significantly reduced mortality from infectious diseases (other than tuberculosis), endocrine disorders, nervous system diseases, pneumoconioses, arteriosclerotic heart disease (WM), and all cancers combined. Proportionate cancer mortality analyses found excess cancers of the buccal cavity, larynx, esophagus, stomach, skin (NW), and cervix, and deficits for cancers of the colon, breast, kidney, pancreas (NW), and lymphohematopoietic system. The excess deaths from injuries, respiratory disease, and stomach cancer, and the deficits of colon cancer and arteriosclerotic heart disease among farmworkers, are consistent with typical mortality patterns previously observed among farm owner/operators. The excess buccal, laryngeal, esophageal, and cervical cancers, and the deficits of breast cancer and lymphohematopoietic cancers have not generally been observed in studies of farm owner/operators.

A cohort mortality study among workers at a 1,3 butadiene facility

This is a cohort mortality study of 2800 male workers employed at least 6 months between 1943 and 1996 at a 1,3-butadiene monomer production facility. Earlier analyses of mortality for this cohort found statistically significant deficits for the ‘all causes of death’ category, and a lower than expected mortality for most leading causes of death. Past analyses also showed a significant elevation for deaths from cancers of the lymphohematopoietic system that was mainly due to an increase in deaths from lymphosarcoma. The purpose of this update was to examine the patterns of mortality through the end of 1999, for five additional years of follow-up. Persons who had become eligible between the last cohort update and April 1996 were added. Cohort membership was closed after April 1996 due to the sale of the facility. A total of 1422 deaths through December 1999 were identified, giving over 200 more deaths than in the last report on this aging cohort. The standardized mortality ratio (SMR) for all causes of death was 89 [95% confidence interval (95% CI) =84–94], which is statistically significantly low, and that for all malignant neoplasms was 90 (95% CI=81–101). The SMR for all lymphohematopoietic cancers (LHC) was 141 (95% CI=105–186) and is statistically significant. The SMR for leukemia was 129 (95% CI=77–204) and for non-Hodgkin's lymphoma (NHL), 148 (95% CI=89–231). The LHC elevations again were found only in workers first employed before 1950 and, in the group with the highest potential for exposure to butadiene, the elevations were highest in the short-term workers. Survival analyses were performed for all LHC [International Classification of Diseases (ICD) codes 200–209], NHL (ICD codes 200, 202), and leukemia (ICD codes 204–207) using an estimate of cumulative butadiene exposure as a time-dependent explanatory variable defined as a combination of job exposure class, calendar time, and length of time in job. The relative risks for the above causes of death were essentially 1.0, suggesting that there was no increase in risk with increasing butadiene exposure.

Dose–response implications of the University of Alabama study of lymphohematopoietic cancer among workers exposed to 1,3-butadiene and styrene in the synthetic rubber industry

New quantitative cancer risk estimates for exposure to 1,3-butadiene are presented. These estimates are based on the most recent human epidemiologic data developed by Drs Delzell and Macaluso and their colleagues at the University of Alabama at Birmingham. The implications of Poisson regression analyses of the relative rate for leukemia are explored using their updated dose estimates and lymphohematopoietic cancer data. The Poisson regression model in these analyses has the same form as in the U.S. Environmental Protection Agency (EPA)'s draft risk assessment of 1,3-butadiene [U.S. Environmental Protection Agency, Health Risk Assessment of 1,3-Butadiene — External Review Draft, National Center for Environmental Assessment, Office of Research and Development, 63 Fed. Reg. 7167 (February 12, 1998) Publication NCEA-W-0267, Washington, 1998]. Consistent with the proposed cancer risk assessment guidelines of the EPA and the EPA's draft risk assessment, the exploration includes the maximum likelihood estimate of the ‘effective concentration’ (EC 01) corresponding to an extra risk of leukemia of 0.01 (1%) from a lifetime continuous exposure to 1,3-butadiene based on a linear dose–response model and the cumulative 1,3-butadiene dose metric (ppm-years). The incorporation of the most recent exposure estimates results in a 2.5-fold decrease in the estimates of leukemia risks computed by EPA. In addition, three changes proposed by the American Chemistry Council (formerly the Chemical Manufacturers Association) to the EPA's Science Advisory Board (SAB) for EPA's draft risk assessment of 1,3-butadiene are incorporated into the calculation. This results in approximately an additional fivefold decrease in the risk estimates of leukemia. The leukemia cancer risk estimates in the EPA's draft risk assessment of 1,3-butadiene decrease by approximately a factor of 13-fold when the updated epidemiologic data and the alternative numbers proposed by industry to the SAB are both incorporated. Specifically, the maximum likelihood estimate of the EC 01 increases from EPA's 1.2 ppm to 2.8 ppm on the basis of the updated epidemiologic data and increases further to 15.1 ppm when the CMA's proposed changes are also incorporated.

Trichloroethylene: Using New Information To Improve the Cancer Characterization

The views expressed in this paper are those of the authors and do not necessarily reflect the views or policies of the U.S. Environmental Protection Agency.Assessments of TCE's potential to cause cancer in humans have had to address issues concerning the strength of the human evidence and the relevance of the animal tumors to humans. The epidemiological database now includes analyses of multiple studies and molecular information. A recent analysis strongly suggests that TCE may induce cancer in humans at multiple sites, including kidney, liver, and lympho-hematopoietic cancer. Molecular analyses have found mutations of the von Hippel-Lindau tumor suppressor gene in renal tumors of TCE-exposed individuals. The animal bioassays have been followed up with mechanistic studies that provide insight into TCE's possible modes of action at each tumor site. This information suggests that TCE may act through mechanisms that can be relevant to human cancers. The mechanistic information can also be used to identify risk factors that may make some people more susceptible to TCE's adverse effects, allowing a fuller characterization of TCE's cancer potential in different groups of people.

A mortality, morbidity, and hematology study of petrochemical employees potentially exposed to 1,3-butadiene monomer

This three-part study is an update of a previous report that examined the mortality, morbidity, and hematological data of employees from a petrochemical facility in Texas who had potential exposure to 1,3-butadiene monomer. The first part describes the updated cause-specific mortality of 614 workers. Vital status for each cohort member was ascertained through 1998, a 9-year extension of the previous study. The second part is an examination of the morbidity experience of cohort members who were still working during 1992–1998, including 289 of the 614 mortality cohort members. The third part is an evaluation of the hematological results from routine health surveillance and/or medical examinations. Approximately 430 of the 614 employees who had complete blood count (CBC) data as of December 1999 were included in the hematological evaluations. The most recent examination containing CBC data was used and compared with similar data for over 2600 other employees from this facility. Overall mortality during the follow-up period, 1948–1998, was significantly lower than for the local comparison population (standardized mortality ratio (SMR) of 0.55 with a 95% confidence interval (CI) of 0.42–0.70). Mortality for all cancer was also significantly lower (SMR, 0.57; 95% CI, 0.32–0.92). Mortality for all lymphohematopoietic cancer was about the same as the comparison population (SMR, 1.06; 95% CI, 0.22–3.11). None of the cause-specific morbidity was in excess compared with an internal comparison group. There were no differences in the distribution or mean values of heamatological variables (e.g. white blood cells, red blood cells, hemoglobin, platelets, mean corpuscular volume) between the butadiene cohort and the comparison group, or between a subgroup of workers in jobs with the highest potential for butadiene exposure (i.e. shipping) and the rest of the butadiene cohort. The findings of this study suggest that the butadiene exposure at this facility in the last 20 years does not pose a health hazard to employees.

Estimating mean exposures from censored data: exposure to benzene in the Australian petroleum industry

A retrospective assessment of exposure to benzene was carried out for a nested case control study of lympho-haematopoietic cancers, including leukaemia, in the Australian petroleum industry. Each job or task in the industry was assigned a Base Estimate (BE) of exposure derived from task-based personal exposure assessments carried out by the company occupational hygienists. The BEs corresponded to the estimated arithmetic mean exposure to benzene for each job or task and were used in a deterministic algorithm to estimate the exposure of subjects in the study.Nearly all of the data sets underlying the BEs were found to contain some values below the limit of detection (LOD) of the sampling and analytical methods and some were very heavily censored; up to 95% of the data were below the LOD in some data sets. It was necessary, therefore, to use a method of calculating the arithmetic mean exposures that took into account the censored data.Three different methods were employed in an attempt to select the most appropriate method for the particular data in the study. A common method is to replace the missing (censored) values with half the detection limit. This method has been recommended for data sets where much of the data are below the limit of detection or where the data are highly skewed; with a geometric standard deviation of 3 or more. Another method, involving replacing the censored data with the limit of detection divided by the square root of 2, has been recommended when relatively few data are below the detection limit or where data are not highly skewed. A third method that was examined is Cohen's method. This involves mathematical extrapolation of the left-hand tail of the distribution, based on the distribution of the uncensored data, and calculation of the maximum likelihood estimate of the arithmetic mean.When these three methods were applied to the data in this study it was found that the first two simple methods give similar results in most cases. Cohen's method on the other hand, gave results that were generally, but not always, higher than simpler methods and in some cases gave extremely high and even implausible estimates of the mean. It appears that if the data deviate substantially from a simple log-normal distribution, particularly if high outliers are present, then Cohen's method produces erratic and unreliable estimates. After examining these results, and both the distributions and proportions of censored data, it was decided that the half limit of detection method was most suitable in this particular study.

Estimating mean exposures from censored data: exposure to benzene in the Australian petroleum industry

A retrospective assessment of exposure to benzene was carried out for a nested case control study of lympho-haematopoietic cancers, including leukaemia, in the Australian petroleum industry. Each job or task in the industry was assigned a Base Estimate (BE) of exposure derived from task-based personal exposure assessments carried out by the company occupational hygienists. The BEs corresponded to the estimated arithmetic mean exposure to benzene for each job or task and were used in a deterministic algorithm to estimate the exposure of subjects in the study. Nearly all of the data sets underlying the BEs were found to contain some values below the limit of detection (LOD) of the sampling and analytical methods and some were very heavily censored; up to 95% of the data were below the LOD in some data sets. It was necessary, therefore, to use a method of calculating the arithmetic mean exposures that took into account the censored data. Three different methods were employed in an attempt to select the most appropriate method for the particular data in the study. A common method is to replace the missing (censored) values with half the detection limit. This method has been recommended for data sets where much of the data are below the limit of detection or where the data are highly skewed; with a geometric standard deviation of 3 or more. Another method, involving replacing the censored data with the limit of detection divided by the square root of 2, has been recommended when relatively few data are below the detection limit or where data are not highly skewed. A third method that was examined is Cohen's method. This involves mathematical extrapolation of the left-hand tail of the distribution, based on the distribution of the uncensored data, and calculation of the maximum likelihood estimate of the arithmetic mean. When these three methods were applied to the data in this study it was found that the first two simple methods give similar results in most cases. Cohen's method on the other hand, gave results that were generally, but not always, higher than simpler methods and in some cases gave extremely high and even implausible estimates of the mean. It appears that if the data deviate substantially from a simple log-normal distribution, particularly if high outliers are present, then Cohen's method produces erratic and unreliable estimates. After examining these results, and both the distributions and proportions of censored data, it was decided that the half limit of detection method was most suitable in this particular study.

Validation of exposure estimation for benzene in the Australian petroleum industry.

A nested case-control study was undertaken to investigate whether an excess of lympho-haematopoietic cancers in the Australian petroleum industry was associated with benzene exposure. The benzene exposures of the cases and controls were estimated using a quantitative algorithm based largely on exposures measured in the Australian petroleum industry. The algorithm was used to estimate, for each subject, the benzene exposure in parts per million (ppm) for each job held in the industry, and the cumulative exposure in ppm years. Because of the critical importance of the exposure assessment in this design of epidemiological study, particular attention was paid to the reliability of the inputs to the algorithm. The inputs [base estimates (BEs) of exposure and technology-specific exposure modifiers (EMs)] were compared to data from other sources including the occupational hygiene literature. Where such comparison data were available, they were generally found to confirm the values used in the algorithm, although four input values were changed as a result of the validation exercise. The integrity of the task-based algorithm was validated by employing it to calculate the exposures of the tanker drivers in the study and comparing these with measured daily exposure for tanker drivers in the Australian petroleum industry and exposure values found in the occupational hygiene literature. After adjustment for the mix of products carried by the Australian tanker drivers, the estimates from the algorithm were found to be comparable to the measured and literature values. This exercise provided evidence that the exposure assessment for the epidemiological study was reliable and that the results of the study can be used as the basis for evaluating the relationship between exposure to benzene and the risk of lympho-haematopoietic cancer.

Retrospective exposure assessment for benzene in the Australian petroleum industry

An excess of lympho-haematopoietic (LH) cancers has been identified in the Australian petroleum industry through the Health Watch surveillance programme. A nested case-control study is being conducted to investigate this excess. This paper describes the methods used to provide quantitative estimates of benzene exposure for each of the subjects in the case-control study. Job histories were compiled for each subject from interviews and company employment records. Site visits and telephone interviews were used to identify the tasks included in each job title. Details about the tasks such as their frequency, the technology in use and about changes that had taken place over the years were also gathered. Exposure dated back to the late 1940s for a few subjects. Collaborating petroleum companies provided recent benzene exposure monitoring data. These were used to generate Base Estimates of exposure for each task, augmented with data from the literature where necessary. Past exposures were estimated from the Base Estimates by means of an exposure algorithm. The modifying effects of technological changes and changes to the product were used in the algorithm. The algorithm was then computed to give, for each job, for each subject, an estimate of average benzene exposure in ppm in the workplace atmosphere (Workplace Estimate). This value was multiplied by the years for which the job was held and these values summed to give an estimate of Cumulative Estimate of benzene in ppm-years. The occupational hygienists performing the exposure assessment did so without knowledge of the case or control status of subjects. Overall exposures to benzene in the Australian petroleum industry were low, and virtually all activities and jobs were below a time-weighted average of 5 ppm. Exposures in terminals were generally higher than at refineries. Exposures in upstream areas were extremely low. Estimates of Cumulative Estimate to benzene ranged from 0.005 to 50.9 ppm-years.

Retrospective exposure assessment for benzene in the Australian petroleum industry

An excess of lympho-haematopoietic (LH) cancers has been identified in the Australian petroleum industry through the Health Watch surveillance programme. A nested case-control study is being conducted to investigate this excess. This paper describes the methods used to provide quantitative estimates of benzene exposure for each of the subjects in the case-control study.Job histories were compiled for each subject from interviews and company employment records. Site visits and telephone interviews were used to identify the tasks included in each job title. Details about the tasks such as their frequency, the technology in use and about changes that had taken place over the years were also gathered. Exposure dated back to the late 1940s for a few subjects.Collaborating petroleum companies provided recent benzene exposure monitoring data. These were used to generate Base Estimates of exposure for each task, augmented with data from the literature where necessary. Past exposures were estimated from the Base Estimates by means of an exposure algorithm. The modifying effects of technological changes and changes to the product were used in the algorithm.The algorithm was then computed to give, for each job, for each subject, an estimate of average benzene exposure in ppm in the workplace atmosphere (Workplace Estimate). This value was multiplied by the years for which the job was held and these values summed to give an estimate of Cumulative Estimate of benzene in ppm-years. The occupational hygienists performing the exposure assessment did so without knowledge of the case or control status of subjects.Overall exposures to benzene in the Australian petroleum industry were low, and virtually all activities and jobs were below a time-weighted average of 5ppm. Exposures in terminals were generally higher than at refineries. Exposures in upstream areas were extremely low. Estimates of Cumulative Estimate to benzene ranged from 0.005 to 50.9ppm-years.

Hip and knee implantations among patients with osteoarthritis and risk of cancer: a record-linkage study from Denmark.

A nationwide cohort study of hip and knee replacement patients in Denmark was undertaken to assess any carcinogenic potential of these implants. A cohort of 22,997 osteoarthritis patients who received hip replacements and of 4,771 osteoarthritis patients who received knee replacements during the period 1977 through 1989 were identified using the nationwide Danish Hospital Discharge Registry. These patients were followed for cancer occurrence through 1993, using the Danish Cancer Registry. There was no overall excess of cancer in either the hip implant cohort [standardized incidence ratio (SIR) = 0.94; 95% confidence interval (CI)= 0.91-0.98] or the knee implant cohort (SIR = 0.97; 95% CI = 0.89-1.06). The risk reduction in both groups of patients reflected for the most part reduced risks for cancers of the respiratory system and the digestive tract, particularly stomach cancer (SIR = 0.69; 95% CI = 0.50-0.81 for hip replacement patients; SIR = 0.46; 95% CI = 0.20-0.91 for knee replacement patients). Elevated risks were observed for melanoma of the skin in both groups of patients. There was no clear excess risk for lymphohematopoietic cancers or malignant neoplasms of the bone or connective tissue among implant patients in either implant group. Contrary to an earlier study in Sweden, we did not find an excess risk for kidney or prostate cancers. In summary, these nationwide results indicate no overall cancer hazard among hip and knee implant patients, but limited follow-up warrants continued surveillance of individuals undergoing these increasingly common surgical procedures.

Cancer in asbestos-exposed occupational cohorts: a meta-analysis.

To examine existing asbestos-exposed occupational cohorts and apply a meta-analytic technique to determine the magnitude of association between exposure and lung cancer and to investigate other cancer sites that may be related to such an exposure. We summarized the data from 69 asbestos-exposed occupational cohorts reporting on cancer morbidity and mortality. Data were extracted regarding numbers of deaths for each cancer, numbers of mesotheliomas, occupations and latency for respiratory, gastrointestinal, urinary and lymphohematopoietic cancers. For each cancer, we calculated a meta-SMR and examined heterogeneity of results using a chi-square test and by calculating a Z-statistic for each study. To examine the dose-response effect, we divided the studies into tertiles according to the percentage of mesothelioma deaths that served as a proxy estimation of asbestos exposure. Lung cancer data demonstrated meta-SMRs of 163 and 148 with and without latency, respectively, with significant heterogeneity of results even after stratification according to occupational groups. Stratification of lung cancer studies according to percentage of mesothelioma deaths showed a dose-response effect. Z-scores ranged from -12.21 to + 29.49. Analysis for laryngeal cancer yielded meta-SMRs of 157 and 133 with and without latency, respectively, demonstrating homogeneous results across studies but accompanied by no evidence of a dose-response effect. Data for gastrointestinal cancers showed no evidence of a significant association and no dose-response effect. Kidney cancer demonstrated statistically non-significant meta-SMRs of 120 (95% CI 88-160) and 111 (95% CI 94-131) with and without latency respectively. This meta-analysis demonstrates a wide variability of the association between occupational asbestos and lung cancer. There was a suggestion of an association between asbestos and laryngeal carcinoma and no clear association with other cancers.

Small area study of mortality among people living near multiple sources of air pollution.

OBJECTIVE: In the area of Malagrotta, a suburb of Rome (Italy), a large waste disposal site, a waste incinerator plant, and an oil refinery plant became operational in the early...