Past Asbestos Exposure Research Articles

Solid Cancer Mortality Associated with Chronic External Radiation Exposure at the French Atomic Energy Commission and Nuclear Fuel Company

Studies of nuclear workers make it possible to directly quantify the risks associated with ionizing radiation exposure at low doses and low dose rates. Studies of the CEA (Commissariat à l'Energie Atomique) and AREVA Nuclear Cycle (AREVA NC) cohort, currently the most informative such group in France, describe the long-term risk to nuclear workers associated with external exposure. Our aim is to assess the risk of mortality from solid cancers among CEA and AREVA NC nuclear workers and its association with external radiation exposure. Standardized mortality ratios (SMRs) were calculated and internal Poisson regressions were conducted, controlling for the main confounding factors [sex, attained age, calendar period, company and socioeconomic status (SES)]. During the period 1968-2004, there were 2,035 solid cancers among the 36,769 CEA-AREVA NC workers. Cumulative external radiation exposure was assessed for the period 1950-2004, and the mean cumulative dose was 12.1 mSv. Mortality rates for all causes and all solid cancers were both significantly lower in this cohort than in the general population. A significant excess of deaths from pleural cancer, not associated with cumulative external dose, was observed, probably due to past asbestos exposure. We observed a significant excess of melanoma, also unassociated with dose. Although cumulative external dose was not associated with mortality from all solid cancers, the central estimated excess relative risk (ERR) per Sv of 0.46 for solid cancer mortality was higher than the 0.26 calculated for male Hiroshima and Nagasaki A-bomb survivors 50 years or older and exposed at the age of 30 years or older. The modification of our results after stratification for SES demonstrates the importance of this characteristic in occupational studies, because it makes it possible to take class-based lifestyle differences into account, at least partly. These results show the great potential of a further joint international study of nuclear workers, which should improve knowledge about the risks associated with chronic low doses and provide useful risk estimates for radiation protection.

Osteopontin, asbestos exposure and pleural plaques: a cross-sectional study

BackgroundOsteopontin (OPN) is a plasma protein/cytokine produced in excess in several malignancies. In a recent study OPN was reported as being related to the duration of asbestos exposure and presence of benign asbestos-related diseases; however, it was unclear whether this protein was an indicator of exposure or effect.MethodsIn 193 workers, 50 with pleural plaques (PP), in whom different indicators of past asbestos exposure were estimated, OPN plasma levels were assessed using commercial quantitative sandwich enzyme immunoassays according to the manufacturer's instructions.ResultsOsteopontin increased with increasing age and several aspects of asbestos exposure, without differences related to the presence of pleural plaques. At multivariable regression analysis, the explanatory variables with a significant independent influence on OPN were length of exposure (positive correlation) and time elapsed since last exposure (positive correlation).ConclusionsSince asbestos in lung tissue tends to wane over time, OPN should decrease (rather than increase) with time since last exposure. Therefore, OPN cannot be a reliable biomarker of exposure nor effect (presence of pleural plaques).

Syntenic Relationships between Genomic Profiles of Fiber-Induced Murine and Human Malignant Mesothelioma

Malignant mesothelioma (MM) is an aggressive tumor with a poor prognosis mainly linked to past asbestos exposure. Murine models of MM based on fiber exposure have been developed to elucidate the mechanism of mesothelioma formation. Genomic alterations in murine MM have now been partially characterized. To gain insight into the pathophysiology of mesothelioma, 16 murine and 35 human mesotheliomas were characterized by array-comparative genomic hybridization and were screened for common genomic alterations. Alteration of the 9p21 human region, often by biallelic deletion, was the most frequent alteration in both species, in agreement with the CDKN2A/CDKN2B locus deletion in human disease and murine models. Other shared aberrations were losses of 1p36.3-p35 and 13q14-q33 and gains of 5p15.3-p13 regions. However, some differences were noted, such as absence of recurrent alterations in mouse regions corresponding to human chromosome 22. Comparison between altered recurrent regions in asbestos-exposed and non-asbestos-exposed patients showed a significant difference in the 14q11.2-q21 region, which was also lost in fiber-induced murine mesothelioma. A correlation was also demonstrated between genomic instability and tumorigenicity of human mesothelioma xenografts in nude mice. Overall, these data show similarities between murine and human disease, and contribute to the understanding of the influence of fibers in the pathogenesis of mesothelioma and validation of the murine model for preclinical testing.

P69 Mesothelioma in the 21st century. A 1-year survey of malignant mesothelioma in the South West of the UK

Introduction Malignant mesothelioma (MM) is a cancer that most commonly arises within the pleura, and carries a poor prognosis. There is a strong association with past asbestos exposure so incidence varies across the UK. In the South West of the UK there is a high incidence with many cases being due to asbestos exposure in the ship-building industry. Aims To describe the demographics, treatment strategies and survival of patients presenting with MM across the Peninsula cancer network, a population of around 1.7 million people, over a 1-year period. Method Cases of MM diagnosed in 2007 were identified retrospectively and reviewed following interrogation of cancer, MDT, pathology and post mortem databases for the five hospitals in the network. A full review of the clinical records was performed. Results 81 patients were identified. Average age was 72 and 94% were male. 82.7% of patients had a performance status of 0 or 1 at presentation but 21% had a significant co-morbidity, most commonly cardiac in nature. 77.8% of patients had definite or probable asbestos exposure. At presentation symptoms had been present for a mean of 3.7 months, the commonest being breathlessness and chest pain. A definitive diagnosis was made in 84% of patients, either on histology (75%) or cytology (9%) and the epithelioid subtype was most common (40.7% of cases). VATS was the main diagnostic modality (61.7%). Despite 61.7% of patients technically being fit for chemotherapy, only 29.6% received it. Mean survival was 269 days (8.8 months). Survival was longer in those with a better performance status at presentation (PS0=344 days, PS1=270d, PS2=125d, PS3=89d), and in those who received chemotherapy (448d vs 269d). Conclusion MM remains a common problem in the South West of the UK. Despite recent treatment advances the prognosis remains poor, with our survival data being similar to that described in earlier population based studies and in chemotherapy treatment trials. Only a small proportion of our patients received chemotherapy and this may reflect the lack of NICE guidance for use of pemetrexed which was only issued in 2008. However, those patients who recieved chemotherapy had a better survival time (14.7 months vs 8.8 month).

The Precautionary Principle: Radiofrequency Exposures from Mobile Telephones and Base Stations

Dolan and Rowley (2009) reported that the precautionary principle “is not appropriate to policy on the use of mobile telephones and the siting of base stations” because there is no established health hazard from the exposure to low-dose radiation. The guidelines [International Commission on Non-Ionizing Radiation Protection (ICNIRP) 1998] provide guidance on protection only from thermal effects (when an increase in body temperature causes injury to the tissue for a short period of time). These guidelines do not cover effects on humans or the environment from nonthermal effects [i.e., effects from electromagnetic fields (EMF) or chronic exposure that do not increase body temperature]. These nonthermal effects of EMF have been well documented by Belyaev (2005) and Sage et. al. (2007). Therefore, the precautionary principle is needed to protect the environment from these effects. Several reports have recommended use of the precautionary principle for these exposures [Herberman 2008; International Commission for Electromagnetic Safety (ICEMS) 2006, 2008; Russian National Committee on Non-Ionizing Radiation Protection 2008; Sage et al. 2007]. I do not agree with Dolan and Rowley (2009) that there is no plausible hazard to humans from the exposure to low-dose radiation. Clinical diseases caused by environmental exposures develop after a long period of biochemical changes; during this time, the exposed individual may or may not have symptoms. For example, in stomach cancer, biochemical changes may occur 10–20 years before the appearance of the cancer. Dolan and Rowley (2009) also stated that risks can be seen with other activities such as “transport (including aviation) and hot showers.” These risks result from the individual’s choices and are not comparable to exposure to electromagnetic radiation from base stations, which is a constant, chronic exposure that occurs without the individual’s knowledge and permission. The past has taught us many lessons about risk from environmental exposures. For example, the lack of full scientific proof concerning the adverse effects of asbestos and the delay of precautionary action had devasting consequencies to human health [World Commission on the Ethics of Scientific Knowledge and Technology (COMEST) 2005]. If asbestos had been banned in 1965, when the effects of asbestos on mesothelioma were plausible but unproven, the Netherlands alone would have saved approximately 52,000 victims and €30 billion for 1969–2030. An estimated 250,000–400,000 deaths from mesothelioma, lung cancer, and asbestosis caused by past asbestos exposure will occur the next 35 years in the European Union (COMEST 2005). In conclusion, concerning the exposure to electromagnetic fields, the precautionary principle should be applied to protect humans from environmental effects of non-thermal mechanisms.

Synchronous malignant pleural mesothelioma and pulmonary carcinoma in a woman without evidence of asbestos exposure

The synchronous development of malignant mesothelioma and pulmonary carcinoma is extremely rare. In this case, an 83-year-old woman, without evidence of past asbestos exposure, developed malignant pleural mesothelioma and pulmonary adenocarcinoma. She was discovered to have a lung lesion on an unrelated preoperative chest X-ray. Clinical evaluation suggested primary bronchogenic malignancy. She had a forty pack-year smoking history, but quit twenty years previously. At surgery, she had nodularity of the pleura. Pathology revealed adenocarcinoma of the lung and suspected malignant mesothelioma of the pleura. Malignant mesothelioma was confirmed histologically at a second surgery.

Asbestos fiber concentration in the area surrounding a former asbestos cement plant and excess mesothelioma deaths in residents

Many persons who had lived near a former asbestos cement plant (AC plant) died from mesothelioma in Amagasaki city, Japan. Asbestos fiber concentration in the area surrounding the AC plant was estimated so that the female mesothelioma death number predicted by a mathematical model was the same as the observed excess death number. We used the estimated asbestos fiber concentration to predict the excess mesothelioma deaths from 1970 to 2049. In a grid just south of the AC plant, the fiber concentration was estimated to be more than 3 f/ml for K(M) (asbestos potency factor for mesothelioma) of 7.75 x 10(-9). An uncertainty factor of five yields a K(M) range 1.55 x 10(-9) to 38.8 x 10(-9); these in turn correspond to fiber concentrations of 15 and 0.6 f/ml. For K(M) = 7.75 x 10(-9), grid units with higher fiber concentrations than 0.01 f/ml were estimated to extend 4.1 km (95% CI: 3.8-4.4 km) south-southwest of the plant. Over the 80-year study period (1970 to 2049), we predicted that the exposure under study will cause 346 excess mesothelioma deaths with range of 296 to 382 deaths. This prediction suggests that considerable medical resources will be needed through 2049 as a result of past asbestos exposure in this region.

Serum Levels of Soluble Mesothelin-Related Peptides in Malignant and Nonmalignant Asbestos-Related Pleural Disease: Relation with Past Asbestos Exposure

Malignant pleural mesothelioma (MPM) results from malignant transformation of mesothelial cells. Past asbestos exposure represents a major risk factor for MPM and other benign pleural disease. Soluble mesothelin-related peptides (SMRP) have been regarded as a promising serum biomarker for MPM. The aim of this study was to investigate serum levels of SMRP in malignant and nonmalignant asbestos-related pleural disease. Four groups of patients were investigated: group 1 composed of 48 healthy subjects, group 2 composed of 177 patients with previous asbestos exposure and no pleural disease, group 3 composed of 36 patients with MPM, and group 4 composed of 101 patients with previous asbestos exposure and benign pleural disease. Serum SMRP levels were determined by ELISA. Serum SMRP levels were significantly higher among group 3 than the other three groups. There were no differences in SMRP concentrations between groups 2 and 4. Subjects exposed to asbestos had higher SMRP concentrations than normal control subjects regardless of the presence of pleural disease. The area under the receiver operating characteristic curve for SMRP values was 0.75 (95% confidence interval, 0.68-0.83). The SMRP level at 0.55 nmol/L/L was determined as the most optimal cutoff value with resulting sensitivity and specificity of 72% and 72% for the diagnosis of MPM. These data attest to good diagnostic sensitivity and specificity of SMRP for the diagnosis of malignant mesothelioma. We have also shown that serum SMRP levels might serve as a marker of asbestos exposure.

An evaluation of short-term exposures of brake mechanics to asbestos during automotive and truck brake cleaning and machining activities

Historically, the greatest contributions to airborne asbestos concentrations during brake repair work were likely due to specific, short-duration, dust-generating activities. In this paper, the available short-term asbestos air sampling data for mechanics collected during the cleaning and machining of vehicle brakes are evaluated to determine their impact on both short-term and daily exposures. The high degree of variability and lack of transparency for most of the short-term samples limit their use in reconstructing past asbestos exposures for brake mechanics. However, the data are useful in evaluating how reducing short-term, dust-generating activities reduced long-term exposures, especially for auto brake mechanics. Using the short-term dose data for grinding brake linings from these same studies, in combination with existing time-weighted average (TWA) data collected in decades after grinding was commonplace in rebuilding brake shoes, an average 8-h TWA of approximately 0.10 f/cc was estimated for auto brake mechanics that performed arc grinding of linings during automobile brake repair (in the 1960s or earlier). In the 1970s and early 1980s, a decline in machining activities led to a decrease in the 8-h TWA to approximately 0.063 f/cc. Improved cleaning methods in the late 1980s further reduced the 8-h TWA for most brake mechanics to about 0.0021 f/cc. It is noteworthy that when compared with the original OSHA excursion level, only 15 of the more than 300 short-term concentrations for brake mechanics measured during the 1970s and 1980s possibly exceeded the standard. Considering exposure duration, none of the short-term exposures were above the current OSHA excursion level.

Cancers respiratoires professionnels

Lung cancer and pleural mesothelioma are the most common occupational cancers. Recent epidemiological studies have estimated that the fraction attributable to occupational factors varies from 13 to 29% for lung cancer in men and is about 85% for pleural mesothelioma in men. Previous occupational exposure to asbestos is the most common occupational exposure in these cancers. Mesothelioma immediately leads the clinician to look for past asbestos exposure. In contrast, the search for an occupational exposure that should be routine in all cases of lung cancer, is generally more difficult because of the number of occupational aetiological factors and the absence of criteria that allow distinction of an occupational cancer from a tobacco related one. Therefore attention should be paid to the identification of occupational exposure in order to set up primary prevention programmes to prevent exposure still present in the working environment and, on the other hand, to identify the subjects entitled to the acknowledgement of occupational disease and/or to obtain the compensation available to asbestos victims.

Grand Rounds: Asbestos-Related Pericarditis in a Boiler Operator

ContextOccupational and environmental exposures to asbestos remain a public health problem even in developed countries. Because of the long latency in asbestos-related pathology, past asbestos exposure continues to contribute to incident disease. Asbestos most commonly produces pulmonary pathology, with asbestos-related pleural disease as the most common manifestation. Although the pleurae and pericardium share certain histologic characteristics, asbestos-related pericarditis is rarely reported.Case presentationWe present a 59-year-old man who worked around boilers for almost 30 years and was eventually determined to have calcific, constrictive pericarditis. He initially presented with an infectious exacerbation of chronic bronchitis. Chest radiographs demonstrated pleural and pericardial calcifications. Further evaluation with cardiac catheterization showed a hemodynamic picture consistent with constrictive pericarditis. A high-resolution computerized tomography scan of the chest demonstrated dense calcification in the pericardium, right pleural thickening and nodularity, right pleural plaque without calcification, and density in the right middle lobe. Pulmonary function testing showed mild obstruction and borderline low diffusing capacity.DiscussionBased on the patient’s occupational history, the presence of pleural pathology consistent with asbestos, previous evidence that asbestos can affect the pericardium, and absence of other likely explanations, we concluded that his pericarditis was asbestos-related.Relevance to clinical practiceSimilar to pleural thickening and plaque formation, asbestos may cause progressive fibrosis of the pericardium.

Measurement of Asbestos Fibre Concentrations in Fluid of Repeated Bronchoalveolar Lavages of Exposed Workers

The aim of this study was to assess the reliability of asbestos fibre concentration in bronchoalveolar lavage fluid (BALF) by carrying out the mineralogical analysis of BALF at different times in the same patient and comparing the results. Twenty two patients underwent diagnostic fibreoptic bronchoscopy twice: the first was to assess the past asbestos exposure and the second for different clinical reasons. Mineralogical analysis of BALF was carried out. In 16 patients (72.7%), a reduction of concentration in BALF of all asbestos fibres was observed. The concentrations of both chrysotile and amphiboles in the first bronchoalveolar lavage (BAL) were related to their concentrations in the second BAL and the observed differences were not statistically significant. A significant decrease in asbestos body concentration between the first and the second BAL was found (Wilcoxon test, P < 0.01). The reliability of the fibre concentration in BALF as a marker of past asbestos exposure seems quite good. In most cases, it allows us to distinguish workers in different classes of exposure and gives useful information on the pattern of exposure. Uncertainties related in general to lung residues and in particular to mineralogical analysis of BALF (mainly due to the high coefficient of variation (CV) at low fibre concentrations and the results of the statistical analysis on total fibres) suggest that this biomarker is more likely suitable for a qualitative/categorical approach to exposure assessment than a quantitative one.

Determining the Burden of Mesothelioma Mortality: An Investigation of Changes in Cause of Death Coding on the British Mesothelioma Register

P-742 Introduction: The legacy of heavy past occupational asbestos exposures in Britain is a continuing increase in mesothelioma deaths today. The British mesothelioma register stands as one of the most comprehensive and consistent sources of mesothelioma mortality data for a given nation. It's strength lies in the fact that the criteria for including deaths have been consistently applied for over 35 years since the register was established in 1967. These criteria are based on textual information from death certificates and not on death coding to the International Classification of Disease (ICD) frameworks. In order to help inform meaningful comparisons of British mesothelioma mortality with that for other countries, the coding of the causes of death for mesothelioma register deaths was investigated and compared with national death data for Britain. Methods: Within the time period for each ICD revision, the ICD codes which were most frequently assigned to the underlying cause for those deaths included on the mesothelioma register were identified. The number of mesothelioma register deaths for these disease codes was then tabulated by year of death and sex. National death data for Britain for these same disease groups by year of death and sex was obtained from the Office for National Statistics for comparison. Results: For deaths included on the mesothelioma register prior to coding of cause of death to ICD 10 in 2001, the underlying cause of death was most frequently recorded as pleural cancer, lung cancer, cancer of unspecified site or peritoneal cancer. Prior to 1993 when medical enquiries to clarify causes of death were discontinued, these disease groups consistently accounted for around 55%, 15%, 15% and 5% of mesothelioma register deaths respectively. Around 90% of total pleural cancer deaths in Britain in this period are included on the mesothelioma register. Following the introduction of ICD 10 in 2001, around 95% of mesothelioma register deaths are now coded as mesothelioma (code C45) in the underlying cause. Conclusions: The data support the conclusion that prior to the coding of cause of death to ICD 10 in Britain, deaths recorded as cancer of the pleura do not adequately identify the totality of pleural mesothelioma deaths. Since the introduction of death coding to ICD10 in Britain, deaths coded to mesothelioma in the underlying cause closely match the inclusion criteria for the mesothelioma register.

Cytogenetic and molecular genetic changes in malignant mesothelioma

Malignant mesothelioma (MM) results from the accumulation of a number of acquired genetic events, especially deletions, which lead to the inactivation of multiple onco-suppressor genes in a multistep cascade mechanism. Past asbestos exposure represents the major risk factor for MM, and the link between asbestos fibers and MM has been largely proved by several epidemiologic and experimental studies. Asbestos fibers induce DNA and chromosomal damage. Most MM cases have shown multiple chromosomal abnormalities. Chromosomal losses are more common than gains. The most common cytogenetic abnormality in MM is a deletion in 9p21, the locus of CDKN2A, a tumor suppressor gene (TSG). The deletion of CDKN2A is a negative prognostic factor in MM. Loss of TSG CDKN2A/ p14 ARF is also common in MM and mutations in NF2 occur in approximately half of the cases. Despite the ban on asbestos use in Western countries, the incidence of MM is increasing, and asbestos is still used in developing countries. This epidemiologic situation calls for further research. Ongoing studies are already applying high-throughput genomic profiling methods in MM. Genetic alterations observed in MM may be useful in differential diagnosis between lung cancer and MM, as diagnostic markers or therapeutic targets, and as indicators of premalignancy for primary prevention and health surveillance.

A cancer incidence and mortality study of Dow Chemical Canada Inc. manufacturing sites

Previously, the mortality was reported in a cohort of male workers at an Ontario chemical plant. To expand the cohort and to investigate the mortality and cancer incidence risk among chemical manufacturing sites. We followed 5277 men and 1301 women from 1950 to 1999. Employees experienced lower mortality and cancer incidence rates than the general population for several major causes of death, including heart disease, respiratory cancer and many other cancers. There were no cases of angiosarcoma of the liver. We observed a lower mortality rate of prostate cancer [standardized mortality ratio = 0.79, 95% confidence interval (CI) 0.43-1.32], but a higher incidence rate of prostate cancer [standardized incidence ratio (SIR) = 1.22, 95% CI 1.00-1.48]. Among the Sarnia employees, the incidence of pleural neoplasms was increased (5 observed versus 1.48 expected, SIR = 3.37, 95% CI 1.09-7.86). These cancers were included in the 12 deaths with malignant mesothelioma at Sarnia. Consistent with the earlier report, lower mortality rates were observed for the major classifications of disease and malignant neoplasms. The higher incidence rates of prostate cancer are not readily explainable but may reflect increased screening among current employees and recent retirees. Past asbestos exposure prior to 1980 is probably a contributor to the deaths due to malignant mesothelioma but is not reflected in lung cancer mortality. We find little indication of any other increased rates of mortality or cancer within the overall workforce of these chemical plants.

Estimating the Number of Asbestos-related Lung Cancer Deaths in Great Britain from 1980 to 2000

Inhalation of asbestos fibres is known to cause two main kinds of cancer-mesothelioma and lung cancer. While the vast majority of mesothelioma cases are generally accepted as being caused by asbestos, the proportion of asbestos-related lung cancers is less clear and cannot be determined directly because cases are not clinically distinguishable from those due to other causes. The aim of this study was to estimate the number of asbestos-related lung cancers among males by modelling their relative lung cancer mortality among occupations within Great Britain in terms of smoking habits, mesothelioma mortality (as an index of asbestos exposure) and occupation type (as a proxy for socio-economic factors). Proportional mortality ratios for lung cancer and mesothelioma for the 20-year period from 1980 to 2000 (excluding 1981) were calculated for occupational groups. Smoking indicators were developed from three General Household Surveys carried out during the 1980s and 1990s. Poisson regression models were used to estimate the number of asbestos-related lung cancers by estimating the number of lung cancer deaths in each occupation assuming no asbestos exposure and subtracting this from the actual predicted number of lung cancer deaths. The effect of asbestos exposure in predicting lung cancer mortality was weak in comparison to smoking habits and occupation type. The proportion of current smokers in occupational groups and average age at which they started smoking were particularly important factors. Our estimate of the number of asbestos-related lung cancers was between two-thirds and one death for every mesothelioma death: equivalent to between 11 500 and 16 500 deaths during the time period studied. Asbestos-related lung cancer is likely to have accounted for 2-3% of all lung cancer deaths among males in Great Britain over the last two decades of the 20th century. Asbestos-related lung cancers are likely to remain an important component of the total number of lung cancer deaths in the future as part of the legacy of past asbestos exposures in occupational settings.

Corporate interests as an obstacle to the primary prevention of cancer

Corporate interests as an obstacle to the primary prevention of cancer

Pathogenesis of malignant pleural mesothelioma

Malignant pleural mesothelioma (MPM) results from neoplastic transformation of mesothelial cells. Past asbestos exposure represents the major risk factor for MPM, as the link between asbestos fibres and MPM has been largely proved by epidemiological and experimental studies. Asbestos fibres induce DNA and chromosome damage linked to oxidative stress following phagocytosis. Recently, simian virus 40 (SV40) has been implicated in the aetiology of MPM. The origin of human infection has been associated with SV40-contaminated polio vaccines, although to date, no epidemiological data supports this hypothesis. SV40 may act as a coactivator of asbestos in mesothelial oncogenesis. The transforming potency of SV40 results from the activity of two viral proteins, large T and small t antigens. SV40 infection stimulates production of growth factors elsewhere implicated in autocrine growth of mesothelioma cells and inactivates RASSF1, a gene silenced in MPM. Roles for ionising radiation, chemicals or genetic factors have also been suggested from the observation of sporadic MPM cases or animal studies. Genetic alterations in the tumour suppressor genes, P16/CDKN2A and neurofibromatosis 2 (NF2), are found both in human MPM and in asbestos-exposed Nf2-deficient mice. MPM is still of great international concern. Despite a ban on asbestos use in Western countries, the incidence of MPM is increasing, due to the long delay between asbestos exposure and diagnosis. Moreover, asbestos is still used in developing countries. The implication of other risk factors, especially SV40, supports a need for further research into MPM.

Mortality and cancer incidence in a Swedish art glassworks?an updated cohort study

To study mortality and cancer incidence, in a Swedish art glassworks producing both heavy and semi-crystal glassware, in an extended cohort of workers over a long time period during which some preventive actions had taken place. In the updated study, 1,229 men and women were eligible as cohort members during the period 1964-1997. The observed number of cases was compared with expected numbers, as calculated from cause-, age-, gender- and calendar year-specific national rates for mortality and cancer incidence. Among men only, a significant risk was seen for cancer incidence in the colon and rectum [standardised incidence ratio (SIR) 1.92, 95% confidence interval (CI) 1.05-3.23; 14 cases] and increased, but statistically non-significant, risks were also seen for male cases of tumours in the liver/bile ducts and brain. Among women, statistically non-significant risks were seen for tumours in the liver/bile ducts and in the lymphatic and haematopoietic systems. No increased risk for cancer of the lung was found in this updated study. The risk for cancer in the colon/rectum was slightly increased in all work categories, and the increase was statistically significant among male and female unspecified glassworkers (SIR 3.13, 95% CI 1.35-6.16; five male and three female cases). A statistically significantly increased risk for cancer in the liver/bile ducts was seen among refinement workers (SIR 3.96, 95% CI 1.07-10.14; two male and two female cases). Most of the causes of death associated with an elevated standardised mortality ratio (SMR) in the 1985 cohort resulted in lower SMRs in this updated cohort, maybe as a consequence of preventive actions taken at the glassworks. On the other hand, the risk for cancers in the digestive system seems to remain, perhaps due to past asbestos exposure or inhalation/digestion of larger particles in the ambient air.

Mortality of employees of the United Kingdom Atomic Energy Authority, 1946–97

Background: The workforce of the UK Atomic Energy Authority has been the subject of several previous epidemiological investigations. Aims: To detect and investigate associations between mortality rates and employment in...