Abstract  Quantitative estimates of the risk of lung cancer or mesothelioma in humans from asbestos exposure made by the U. S. Environmental Protection Agency (EPA) make use of estimates of potency factors based on phase-contrast microscopy (PCM) and obtained from cohorts exposed to asbestos in different occupational environments. These potency factors exhibit substantial variability. The most likely reasons for this variability appear to be differences among environments in fiber size and mineralogy not accounted for by PCM.

In this article, the U. S. Environmental Protection Agency (EPA) models for asbestos-related lung cancer and mesothelioma are expanded to allow the potency of fibers to depend upon their mineralogical types and sizes. This is accomplished by positing exposure metrics composed of nonoverlapping fiber categories and assigning each category its own unique potency. These category-specific potencies are estimated in a meta-analysis that fits the expanded models to potencies for lung cancer (K(L)'s) or mesothelioma (K(M)'s) based on PCM that were calculated for multiple epidemiological studies in our previous paper (Berman and Crump, 2008). Epidemiological study-specific estimates of exposures to fibers in the different fiber size categories of an exposure metric are estimated using distributions for fiber size based on transmission electron microscopy (TEM) obtained from the literature and matched to the individual epidemiological studies. The fraction of total asbestos exposure in a given environment respectively represented by chrysotile and amphibole asbestos is also estimated from information in the literature for that environment. Adequate information was found to allow K(L)'s from 15 epidemiological studies and K(M)'s from 11 studies to be included in the meta-analysis.

Since the range of exposure metrics that could be considered was severely restricted by limitations in the published TEM fiber size distributions, it was decided to focus attention on four exposure metrics distinguished by fiber width: "all widths," widths > 0.2 mu m, widths < 0.4 mu m, and widths < 0.2 mu m, each of which has historical relevance. Each such metric defined by width was composed of four categories of fibers: chrysotile or amphibole asbestos with lengths between 5 mu m and 10 mu m or longer than 10 mu m. Using these metrics three parameters were estimated for lung cancer and, separately, for mesothelioma: K(LA), the potency of longer (length > 10 mu m) amphibole fibers; rpc, the potency of pure chrysotile (uncontaminated by amphibole) relative to amphibole asbestos; and rps, the potency of shorter fibers (5 mu m < length < 10 mu m) relative to longer fibers.

For mesothelioma, the hypothesis that chrysotile and amphibole asbestos are equally potent (rpc = 1) was strongly rejected by every metric and the hypothesis that (pure) chrysotile is nonpotent for mesothelioma was not rejected by any metric. Best estimates for the relative potency of chrysotile ranged from zero to about 1/200th that of amphibole asbestos (depending on metric). For lung cancer, the hypothesis that chrysotile and amphibole asbestos are equally potent (rpc = 1) was rejected (p <= .05) by the two metrics based on thin fibers (length < 0.4 mu m and < 0.2 mu m) but not by the metrics based on thicker fibers.

The "all widths" and widths < 0.4 mu m metrics provide the best fits to both the lung cancer and mesothelioma data over the other metrics evaluated, although the improvements are only marginal for lung cancer. That these two metrics provide equivalent (for mesothelioma) and nearly equivalent (for lung cancer) fits to the data suggests that the available data sets may not be sufficiently rich (in variation of exposure characteristics) to fully evaluate the effects of fiber width on potency. Compared to the metric with widths > 0.2 mu m with both rps and rpc fixed at 1 (which is nominally equivalent to the traditional PCM metric), the "all widths" and widths < 0.4 mu m metrics provide substantially better fits for both lung cancer and, especially, mesothelioma.

Although the best estimates of the potency of shorter fibers (5 < length < 10 mu m) is zero for the "all widths" and widths < 0.4 mu m metrics (or a small fraction of that of longer fibers for the widths > 0.2 mu m metric for mesothelioma), the hypothesis that these shorter fibers were nonpotent could not be rejected for any of these metrics. Expansion of these metrics to include a category for fibers with lengths < 5 mu m did not find any consistent evidence for any potency of these shortest fibers for either lung cancer or mesothelioma.

Despite the substantial improvements in fit over that provided by the traditional use of PCM, neither the "all widths" nor the widths < 0.4 mu m metrics (or any of the other metrics evaluated) completely resolve the differences in potency factors estimated in different occupational studies. Unresolved in particular is the discrepancy in potency factors for lung cancer from Quebec chrysotile miners and workers at the Charleston, SC, textile mill, which mainly processed chrysotile from Quebec. A leading hypothesis for this discrepancy is limitations in the fiber size distributions available for this analysis. Dement et al. (2007) recently analyzed by TEM archived air samples from the South Carolina plant to determine a detailed distribution of fiber lengths up to lengths of 40 mu m and greater. If similar data become available for Quebec, perhaps these two size distributions can be used to eliminate the discrepancy between these two studies.

Abstract  The most recent update of the U.S. Environmental Protection Agency (EPA) health assessment document for asbestos (Nicholson, 1986, referred to as “the EPA 1986 update”) is now 20 years old. That document contains estimates of “potency factors” for asbestos in causing lung cancer (KL’s) and mesothelioma (KM’s) derived by fitting mathematical models to data from studies of occupational cohorts. The present paper provides a parallel analysis that incorporates data from studies published since the EPA 1986 update. The EPA lung cancer model assumes that the relative risk varies linearly with cumulative exposure lagged 10 years. This implies that the relative risk remains constant after 10 years from last exposure. The EPA mesothelioma model predicts that the mortality rate from mesothelioma increases linearly with the intensity of exposure and, for a given intensity, increases indefinitely after exposure ceases, approximately as the square of time since first exposure lagged 10 years. These assumptions were evaluated using raw data from cohorts where exposures were principally to chrysotile (South Carolina textile workers, Hein et al., 2007; mesothelioma only data from Quebec miners and millers, Liddell et al., 1997) and crocidolite (Wittenoom Gorge, Australia miners and millers, Berry et al., 2004) and using published data from a cohort exposed to amosite (Paterson, NJ, insulation manufacturers, Seidman et al., 1986). Although the linear EPA model generally provided a good description of exposure response for lung cancer, in some cases it did so only by estimating a large background risk relative to the comparison population. Some of these relative risks seem too large to be due to differences in smoking rates and are probably due at least in part to errors in exposure estimates. There was some equivocal evidence that the relative risk decreased with increasing time since last exposure in theWittenoom cohort, but none either in the South Carolina cohort up to 50 years from last exposure or in the New Jersey cohort up to 35 years from last exposure. The mesothelioma model provided good descriptions of the observed patterns of mortality after exposure ends, with no evidence that risk increases with long times since last exposure at rates that vary from that predicted by the model (i.e., with the square of time). In particular, the model adequately described the mortality rate in Quebec chrysotile miners and millers up through >50 years from last exposure. There was statistically significant evidence in both the Wittenoom and Quebec cohorts that the exposure intensity-response is supralinear1 rather than linear. The best-fitting models predicted that the mortality rate varies as [intensity]0.47 for Wittenoom and as [intensity]0.19 for Quebec and, in both cases, the exponent was significantly less than 1 (p < .0001). Using the EPA models, KL’s and KM’s were estimated from the three sets of raw data and also frompublished data covering a broader range of environments than those originally addressed in the EPA 1986 update. Uncertainty in these estimates was quantified using “uncertainty bounds” that reflect both statistical and nonstatistical uncertainties. Lung cancer potency factors (KL’s) were developed from 20 studies from 18 locations, compared to 13 locations covered in the EPA 1986 update. Mesothelioma potency factors (KM’s) were developed for 12 locations compared to four locations in the EPA 1986 update. Although the 4 locations used to calculate KM in the EPA 1986 update include one location with exposures to amosite and three with exposures to mixed fiber types, the 14 KM’s derived in the present analysis also include 6 locations in which exposures were predominantly to chrysotile and 1 where exposures were only to crocidolite. The KM’s showed evidence of a trend, with lowest KM’s obtained fromcohorts exposed predominantly to chrysotile and highest KM’s from cohorts exposed only to amphibole asbestos, with KM’s from cohorts exposed to mixed fiber types being intermediate between the KM’s obtained from chrysotile and amphibole environments. Despite the considerable uncertainty in the KM estimates, the KM from the Quebec mines and mills was clearly smaller than those from several cohorts exposed to amphibole asbestos or a mixture of amphibole asbestos and chrysotile. For lung cancer, although there is some evidence of larger KL’s fromamphibole asbestos exposure, there is a good deal of dispersion in the data, and one of the largest KL‘s is from the South Carolina textile mill where exposures were almost exclusively to chrysotile. This KL is clearly inconsistent with the KL obtained from the cohort of Quebec chrysotile miners and millers. The KL’s and KM’s derived herein are defined in terms of concentrations of airborne fibers measured by phase-contrast microscopy (PCM), which only counts all structures longer than 5 μm, thicker than about 0.25 μm, and with an aspect ratio ≥3:1. Moreover, PCM does not distinguish between asbestos and nonasbestos particles. One possible reason for the discrepancies between the KL’s and KM’s from different studies is that the category of structures included in PCM counts does not correspond closely to biological activity. In the accompanying article (Berman and Crump, 2008) the KL’s and KM’s and related uncertainty bounds obtained in this article are paired with fiber size distributions from the literature obtained using transmission electron microscopy (TEM). The resulting database is used to define KL’s and KM’s that depend on both the size (e.g., length and width) and mineralogical type (e.g., chrysotile or crocidolite) of an asbestos structure. An analysis is conducted to determine how well different KL and KM definitions are able to reconcile the discrepancies observed herein among values obtained from different environments.

Abstract  BACKGROUND: Previous studies of a cohort of rubber hydrochloride workers indicated an association between benzene exposure and excess mortality from leukemia and multiple myeloma. To determine whether risks remain elevated with increasing time since plant shutdown, we extended follow-up from 1981 through 1996. MATERIALS AND METHODS: We evaluated risk using standardized mortality ratios (SMR) and generalized Cox proportional hazards regression models. RESULTS: Five new leukemia cases were observed in benzene-exposed white males, but the summary SMR for this group declined from 3.37 (95% CI = 1.54-6.41) to 2.56 (95% CI = 1.43-4.22). In regression models, cumulative exposure was significantly associated with elevated relative risks for leukemia mortality. Four new multiple myeloma deaths occurred, three of which were in workers judged to be unexposed. CONCLUSIONS: These findings reaffirm the leukemogenic effects of benzene exposure and suggest that excess risk diminishes with time.

Abstract  Knowledge of mortality patterns following exposure to asbestos has been determined mostly from cohort studies of men who were exposed to asbestos in their workplace. Women are more likely to have obtained their asbestos exposure domestically or from their environment.

2552 women and girls are documented to have lived in the blue asbestos mining and milling township of Wittenoom between 1943 and 1992 and were not involved in asbestos mining or milling. Quantitative asbestos exposure measurements were derived from periodic dust surveys undertaken in the industry and around the township. Death records were obtained for the period 1950-2004. Standardised mortality ratios (SMRs) were calculated to compare the Wittenoom women's mortality with that of the Western Australian female population.

There were 425 deaths, including 30 from malignant mesothelioma. There was excess mortality for all causes of death (SMR = 1.13), all neoplasms (SMR = 1.42), symptoms, signs and ill defined conditions (SMR = 6.35), lung cancer (SMR = 2.15) and pneumoconiosis (SMR = 11.8). Mortality from cancer of the ovary (SMR = 1.52), upper aerodigestive cancers (SMR = 2.70) and tuberculosis (SMR = 5.38) was increased but not significantly. The risk of death from mesothelioma was increased, but not significantly, in residents known to have lived with or washed the clothes of an Australian Blue Asbestos Company asbestos worker (HR = 2.67, 95% CI 0.77 to 9.21; HR = 2.61, 95% CI 0.85 to 7.99, respectively).

Women who were former residents of Wittenoom, exposed to asbestos in their environment or in their home, have excess cancer mortality, including mesothelioma, compared with the Western Australian female population.

Abstract  This report provides an update of the mortality experience of a cohort of South Carolina asbestos textile workers.

A cohort of 3072 workers exposed to chrysotile in a South Carolina asbestos textile plant (1916-77) was followed up for mortality through 2001. Standardised mortality ratios (SMRs) were computed using US and South Carolina mortality rates. A job exposure matrix provided calendar time dependent estimates of chrysotile exposure concentrations. Poisson regression models were fitted for lung cancer and asbestosis. Covariates considered included sex, race, age, calendar time, birth cohort and time since first exposure. Cumulative exposure lags of 5 and 10 years were considered by disregarding exposure in the most recent 5 and 10 years, respectively.

A majority of the cohort was deceased (64%) and 702 of the 1961 deaths occurred since the previous update. Mortality was elevated based on US referent rates for a priori causes of interest including all causes combined (SMR 1.33, 95% CI 1.28 to 1.39); all cancers (SMR 1.27, 95% CI 1.16 to 1.39); oesophageal cancer (SMR 1.87, 95% CI 1.09 to 2.99); lung cancer (SMR 1.95, 95% CI 1.68 to 2.24); ischaemic heart disease (SMR 1.20, 95% CI 1.10 to 1.32); and pneumoconiosis and other respiratory diseases (SMR 4.81, 95% CI 3.84 to 5.94). Mortality remained elevated for these causes when South Carolina referent rates were used. Three cases of mesothelioma were observed among cohort members. Exposure-response modelling for lung cancer, using a linear relative risk model, produced a slope coefficient of 0.0198 (fibre-years/ml) (standard error 0.00496), when cumulative exposure was lagged 10 years. Poisson regression modelling confirmed significant positive relations between estimated chrysotile exposure and lung cancer and asbestosis mortality observed in previous updates of this cohort.

This study confirms the findings from previous investigations of excess mortality from lung cancer and asbestosis and a strong exposure-response relation between estimated exposure to chrysotile and mortality from lung cancer and asbestosis.

Abstract  ICD-9 code 163 (malignant neoplasm of pleura) listed as underlying cause of death detected only 40% of Scottish mesothelioma cases (all body sites) from the cancer registry in 1981-1999. This is lower than both the previously published 55% figure, derived from UK mesothelioma register data 1986-1991, which is based on any mention of mesothelioma on death certificates, cross-referenced to cancer registry data, and the 44% figure derived from Scottish mortality data 1981-1999, which captured any mention of mesothelioma on the death certificate. Detection from cancer registry data increased to 75% under ICD-10 in Scotland, confirming earlier predictions of the benefit of ICD-10's more specific mesothelioma codes. Including the accidental poisoning codes E866.4 (ICD-9) and X49 (ICD-10), covering poisoning by 'unspecified' and 'other' causes, which appear to have been used as coding surrogates for mesothelioma when asbestos exposure was explicitly mentioned in deaths suggestive of a mesothelioma, and which are recorded as the underlying cause of death in 4-7% of mesotheliomas, may improve the mesothelioma detection rate in future epidemiological studies.

Abstract  A cohort of 889 men and 1077 women employed for at least 1 month between 1946 and 1984 by a former Italian leading asbestos (mainly textile) company, characterised by extremely heavy exposures often for short durations, was followed up to 1996, for a total of 53,024 person-years of observation. Employment data were obtained from factory personnel records, while vital status and causes of death were ascertained through municipality registers and local health units. We observed 222 cancer deaths compared with 116.4 expected (standardized mortality ratio, SMR=191). The highest ratios were found for pleural (SMR=4105), peritoneal (SMR=1817) and lung (SMR=282) cancers. We observed direct relationships with duration of employment for lung and peritoneal cancer, and with time since first employment for lung cancer and mesothelioma. Pleural cancer risk was independent from duration (SMR=3428 for employment <1 year, 7659 for 1-4 years, 2979 for 5-9 years and 2130 for > or =10 years). Corresponding SMRs for lung cancer were 139, 251, 233 and 531. Nonsignificantly increased ratios were found for ovarian (SMR=261), laryngeal (SMR=238) and oro-pharyngeal (SMR=226) cancers. This study confirms and further quantifies the central role of latency in pleural mesothelioma and of cumulative exposure in lung cancer.

Abstract  Mining, handling, processing, and personal or commercial use of asbestos-contaminated vermiculite have led to widespread contamination of the Libby, Montana, area. We initiated a medical testing program in response to reports of respiratory illness in the community. The purpose of this analysis was to identify and quantify asbestos-related radiographic abnormalities among persons exposed to vermiculite in Libby and to examine associations between these outcomes and participants' self-reported exposures. A cross-sectional interview and medical testing were conducted in Libby from July through November 2000 and from July through September 2001. A total of 7,307 persons who had lived, worked, or played in Libby for at least 6 months before 31 December 1990 completed the interview. Of those, 6,668 participants > or = 18 years of age received chest radiographs to assess the prevalence of pleural and interstitial abnormalities. We observed pleural abnormalities in 17.8% of participants and interstitial abnormalities in < 1% of participants undergoing chest radiography. We examined 29 occupational, recreational, household, and other exposure pathways in the analysis. The prevalence of pleural abnormalities increased with increasing number of exposure pathways, ranging from 6.7% for those who reported no apparent exposures to 34.6% for those who reported > or = 12 pathways. The factors most strongly associated with pleural abnormalities were being a former W.R. Grace worker, being older, having been a household contact of a W.R. Grace worker, and being a male. In addition to being a former W.R. Grace worker, environmental exposures and other nonoccupational risk factors were also important predictors of asbestos-related radiographic abnormalities.

Abstract  Background: Asbestos inhalation is recognized as an exposure that increases the risk for the development of lung disease. It is unique among dusts in that it is both a carcinogen and capable of inducing extrapulmonary responses such as pleural thickening and fibrosis as well as malignancy. One feature of asbestos suggested as crucial in its pathological activity is its fibrous morphology. Long fibers that have been inhaled are cleared less readily and are thus more persistent in the body. Furthermore certain experimental models link fiber length to levels of risks for development of certain diseases. The present review will survey the data on this subject. Methods: The review considers experimental models that have been used to assess the response to various lengths of fibers in animal models in addition to data obtained from studies of human materials. The review also emphasizes the importance in defining the method by which a sample is categorized. Results: Data are offered which support the potential for longer fibers as well as shorter fibers to contribute to pathological responses. Conclusions: The data presented argue that asbestos fibers of all lengths induce pathological responses and that caution should be exerted when attempting to exclude any population of inhaled fibers, based on their length, from being contributors to the potential for development of asbestos-related diseases.

Abstract  To elucidate the features of the asbestos fibers contributing to the induction of human malignant mesothelioma, we used high-resolution analytical electron microscopy to determine the type, number, and dimensions of asbestos fibers in lung and mesothelial tissues in 168 cases of mesothelioma. Results: 1. Asbestos fibers were present in almost all of the lung and mesothelial tissues from the mesothelioma cases. 2. The most common types of asbestos fibers in lung were either an admixture of chrysotile with amphiboles, amphibole alone, and occasionally chrysotile alone. In mesothelial tissues, most asbestos fibers were chrysotile. 3. In lung, amosite fibers were greatest in number followed by chrysotile, crocidolite, tremolite/actinolite, and anthophyllite. In mesothelial tissues, chrysotile fibers were 30.3 times more common than amphiboles. 4. In some mesothelioma cases, the only asbestos fibers detected in either lung or mesothelial tissue were chrysotile fibers. 5. The average number of asbestos fibers in both lung and mesothelial tissues was two orders of magnitude greater than the number found in the general population. 6. The majority of asbestos fibers in lung and mesothelial tissues were shorter than 5 micro m in length. Conclusions: 1) Fiber analysis of both lung and mesothelial tissues must be done to determine the types of asbestos fibers associated with the induction of human malignant mesothelioma; 2) short, thin asbestos fibers should be included in the list of fiber types contributing to the induction of human malignant mesothelioma; 3) Results support the induction of human malignant mesothelioma by chrysotile.

Abstract  Asbestos fibers in occupationally exposed individuals relocate from the lung to extrapulmonary sites. A mechanism for relocation is via the lymphatic circulation. Indeed, asbestos fibers have been found in lymph nodes as well as pleural plaques. Our laboratory has recently shown that asbestos fibers also reach the mesentery and omentum in the peritoneal area where a small percentage of mesotheliomas occurs in exposed individuals. The present study uses light and analytical transmission electron microscopy for defining the asbestos burden in digested lung, omentum, and mesentery tissues from individuals considered as representing the general population in East Texas. The findings, when compared with previous data from occupationally exposed individuals, indicate extreme contrasts as to the level and types of fiber burden between individuals representing the groups.

Abstract  BACKGROUND: The thoracic lymph nodes are a part of the clearance system from lung tissue. Accumulation of dust in these nodes are known to occur following some types of exposure. However, no information exists as to asbestos content in lymph nodes from the general population. METHODS: The study cohort consisted of 21 individuals previously defined as nonoccupationally exposed to asbestos. Tissue burden of asbestos obtained from lung analysis by analytical electron microscopy was compared with burden in the lymph nodes. RESULTS: No asbestos fibers were detected in nodes from 8 cases. The majority of the fibers found in lymph nodes were short (<5 microm) and most often noncommercial amphiboles. Ferruginous bodies (FBs) were detected in lymph node from only two samples. CONCLUSIONS: The total asbestos burden in the lung tissue from these individuals was quite low. However, in 12 of the 13 cases that had positive nodes, the tissue burden in the node was appreciably heavier per gram than in the lung. This raises the question as to whether the lymph nodes, though less efficient clearance, may be better indicators of lifetime exposure to dust than lung tissue.

Abstract  The primary aim of this prospective study was to examine the tissues and placentas of autopsied stillborn infants for presence of asbestos fibers. Asbestos burden of lung, liver, skeletal muscle, and placenta digests of 82 stillborn infants was determined using standard bleach digestion technique. The digests were examined by electron microscopy, and the types of fibers determined using energy dispersive x-ray analysis and selected area diffraction analysis. Digests of 45 placentas collected from deliveries of liveborn healthy infants were processed and examined similarly as controls. Asbestos fibers were detected in 50% of the fetal digests and 23% of the placental digests of stillborn infants. Of the fibers present, 88% were chrysotile, 10% were tremolite, and 2% were actinolite and anthophyllite. Fibers measured 0.5-16.73 microgram in length (mean 1.55 microgram), and 0.03-0.8 microgram in width (mean 0.098 microgram). Lungs were most frequently positive for fibers (50%), followed by muscle (37%), placenta (23%), and liver (23%). Mean fiber counts were highest in the liver (58,736 f/g), followed by placenta (52,894 f/g), lungs (39,341 f/g), and skeletal muscle (31,733 f/g). Digests of 15% of the control placentas also showed asbestos fibers, although in very small numbers. The mean fiber count of the stillborn placentas (52,894 f/g) was significantly higher than the mean fiber count of the control placentas (mean 19 f/g) (p = 0.001). A highly significant association was found between fiber presence in stillborns and a maternal history of previous abortions (p = 0.007). A significant association was also found between fiber presence and placental diseases (p = 0.041). An association was suggested between working mothers and fiber presence (p = 0.19), although it did not reach statistical significance. The study documents the presence of small and thin asbestos fibers in stillborn fetal tissues and placenta. Significantly higher number of fibers were found in stillborn tissues compared to controls (liveborn placenta). The absence of a maternal history of asbestos-related occupations suggests that the fibers may have been acquired through environmental exposure.

Abstract  The importance of nonoccupational asbestos exposure has been emphasized recently. To illustrate this problem, we report 4 persons with asbestos-related disease from household exposure. There were 2 wives of asbestos workers, who cleaned their husbands' work clothes. One developed a mesothelioma and the other plaques, calcification, benign asbestos pleural effusion and subpleural parenchymal fibrosis. 2 men were exposed as children while playing in a cellar room which was also used for their father's muffler repair business. At ages 27 and 33, they had pleural and diaphragmatic calcifications.

Abstract  Autopsy samples from eight former shipyard workers were collected from lung parenchyma, tracheal lymph nodes, and pleural plaques. The tissue from each respective area was prepared by a modified bleach digestion technique, and the residue was collected on a 0.2-micron pore polycarbonate or 0.22-micron mixed cellulose ester filter. Quantitation of ferruginous bodies and uncoated fibers was done by light and transmission electron microscopy, respectively. Differences in the asbestos burden were noted for each site. Ferruginous bodies were observed in both parenchyma and nodes but not in plaques. Three subjects were found to have more ferruginous bodies per gram dry weight in their lymph nodes than in their lung parenchyma. Likewise, all subjects were found to have more uncoated fibers per gram in the nodes than in the parenchyma. Amphibole and chrysotile fibers were noted in the lung and extrapulmonary sites, with chrysotile being the predominant asbestiform in plaques. The majority of the uncoated fibers in both the nodes and the plaques were less than or equal to 5 microns in length. However, some fibers with dimensions conforming to the "Stanton hypothesis" reached both areas. These residual patterns most likely reflect the impact of clearance on lung burden as opposed to the eventual accumulation and stasis in the extrapulmonary areas.

Abstract  Numerous sources of asbestos exist that may contribute to non-occupational exposures, among the important ones being building surfacing materials that have been damaged or allowed to deteriorate. Even more important is the potential exposure from improperly controlled maintenance activities in buildings. Evidence exists suggesting that vehicle braking makes a significant contribution to ambient asbestos levels, but more data are required to establish its extent. Many asbestos materials are present in homes, and fibres may be released during home renovations or repairs. Little information exists on the levels of other mineral fibres in the non-occupational environment or on the relative contributions from potential sources.

Abstract  Steps taken to implement an asbestos (1332214) operations and maintenance (O) program in New Jersey schools were evaluated. The program utilized appropriate work practices and training to maintain friable asbestos containing materials (ACM) in good condition, ensure proper cleanup of previously released asbestos fibers, and prevent future releases by minimizing and controlling the distribution of ACM during installation, repair, maintenance, and cleaning activities. The program was evaluated at eight schools in New Jersey where O/M activities were in progress or planned. The evaluation was conducted in three phases: a review of each school's program, which was on file with the New Jersey Department of Health; an interview with each school's designated AHERA person to obtain information on the type and location of each O/M activity; and observation and documentation of selected O/M activities involving ACM. Personal air monitoring for asbestos during selected O/M activities was also performed. The samples were analyzed by transmission electron microscopy (TEM) and phase contrast microscopy (PCM). The schools were found not to be implementing all of the elements of the O/M program. Across the eight schools, the percentage performance responses decreased from phase 1 to phase 3. The overall comprehensiveness of the schools' O/M programs varied from 45.9% to 83.8%, average 70.6%. The overall percentage performance responses of the school officials averaged only 52.5%. All elements of the programs were not communicated to the schools' designated AHERA person or the maintenance personnel or outside contractors performing the work. The average percentage performance responses of school maintenance personnel or outside contractors performing the work was only 35% and 22.5%, respectively. TEM showed that O/M activities frequently led to increases in personal air asbestos fiber concentrations above 0.02 seconds per cubic meter, an exposure limit derived from AHERA clearance criteria. PCM found no asbestos fiber concentrations in excess of the OSHA 8 hour time weighted average standard of 0.1 fiber per centimeter. The authors conclude that the selected schools are not currently completely implementing the O/M program.

Abstract  This paper models general survival and the distribution of tumor onset times for various tumors in the data base of control animals developed by the National Toxicology Program. For general survival, a modified Weibull model is shown to give an adequate fit for both Fischer 344 rats and C57BL/6 x C3H F1 mice. In addition, data from control animals in a lifetime study of asbestos are used to support the extension of these survival curves beyond 2 years in Fischer rats. The distributions of tumor onset times are modeled using a two-parameter Weibull model. For many common tumor types, this model yielded a very good fit to the data. Finally, a summary measure of the contribution of a tumor to mortality is given.

Abstract  Mortality and cancer incidence was investigated among the 695 bus garage workers employed as mechanics, servicemen, or hostlers for at least six months in five bus garages in Stockholm between 1945 and 1970. The exposure to diesel exhaust and asbestos was estimated by industrial hygienists. A small excess of lung cancer mortality was found in the cohort when occupationally active men in Stockholm were used as the reference group. A case-referent study was performed within the cohort, six referents being selected for each of the 20 lung cancer cases. The lung cancer risk increased with increasing cumulative exposure to diesel exhaust, but not with cumulative asbestos exposure. The relative risk for lung cancer among the highly exposed men was 2.4 (95% CI 1.3-4.5) as compared with those with low exposure. The study indicates that exposure to diesel exhaust increases the risk for lung cancer.

Abstract  The review of available data on the concentrations of asbestos in U.S. water supplies suggests that the majority of water consumers are not exposed to asbestos concentrations over 1 million fibers/Liter. A few populations, however, may be exposed to concentrations over 1 billion fibers/L. Of the 538 water supplies for which waterborne asbestos data are available, 8% have concentrations of fibers over 10 million fibers/L. The vast majority of asbestos fibers found in U.S. water supplies are under 5 micron in length.

Abstract  Age-adjusted, sex- and race-specific 1969-1971 cancer incidence ratios for the 722 census tracts of the San Francisco-Oakland Standard Metropolitan Statistical Area were compared with measured chysotile asbestos counts in tract drinking waters. The water supplies serving the area have varying contact with naturally occurring serpentine. The t test for multiple regression coefficients and the t test for correlation coefficients showed significant (p less than 0.01) relationships between chrysotile asbestos content of tract drinking water and white male lung, white female gall bladder and pancreas, and peritoneal cancers in both sexes. Of weaker significance (0.01 less than or equal to 0.05) were female esophagus, pleura and kidney, as well as stomach cancers in both sexes. These associations appeared to be independent of income, education, asbestos occupation, marital status, country of origin and mobility.

Abstract  Surveillance of cancer morbidity in Duluth, Minnesota, was undertaken to investigate the effects of ingesting asbestos fibers in municipal drinking water. Tests in 1973 had revealed the presence of 1 to 30 million asbestos-like fibers per liter of tap water. Asbestos-containing taconite ore wastes were dumped into Lake Superior from 1955 to 1980, sometimes at the rate of 67,000 tons per day. Using the methods of the Third National Cancer Survey and comparing results with data collected in Minneapolis and St. Paul showed that Duluth females and both sexes combined had statistically significantly higher rates of pancreatic cancer than persons in Minneapolis and St. Paul for 1969-1971. The rates for both sexes declined during the 1972-1974 period. Morbidity and mortality rates were compared. Mortality rates in Duluth for cancers in certain gastrointestinal sites and for lung cancer were substantially higher for Duluth than for Minneapolis and St. Paul, but morbidity rates were very similar. The time requirements, budget , personnel, and supplies for conducting a morbidity study in a small (100,000) population are described. (Cassar-FRC)

Abstract  A standard tool for the analysis of known and suspected causes of occupational lung cancer in population-based studies is proposed in order to allow comparable definitions of exposure or of categorizations of occupations. It is based on a list of occupations and industries known (list A) or suspected (list B) to be associated with lung cancer. The lists were translated into codes of the International Standard Classification of Occupations (1968) and the International Standard Industrial Classification (1971). The specificity of the categorization is compromised for some groups that are defined by highly specific production processes or exposures. Nevertheless, the grouping is based on a highly valid source of information in population-based studies. It is proposed for use in the assessment of the public health impact of occupational lung cancer.

Abstract  The association of mesothelioma and asbestos exposure is well known, but some data suggest that probably many people are still being exposed to asbestos without knowing it.

Between 1993 and 1996, 132 cases (77% males) of histologically confirmed malignant pleural mesothelioma and 257 controls, residents in two provinces of Spain (Barcelona and C¿adiz), were interviewed. They were classified according to their probability and intensity of occupational asbestos exposure by a panel of industrial hygienists, based on a detailed occupational history.

Age and sex-adjusted odds ratio (OR) for the highest probability of exposure to asbestos was 13.2 (95% confidence interval 6.4-27.3), and 27.1 (9. 28-79.3) for high intensity. A dose-response trend was observed for both, probability and intensity. Overall, 61% of cases and 42% of controls had ever worked in an occupation with risk of asbestos exposure, with an OR of 2.59 (1.60-4.22). In our population 62% of cases could be attributed to occupational asbestos exposure.

A high risk of pleural mesothelioma due to occupational asbestos exposure is confirmed, but there is still a sizeable proportion for which no evidence of occupational exposure was found. Most of these cases could be due to other sources of asbestos exposure, mainly domestic or environmental.

Abstract  From the general population in the county of Uppsala, Sweden, 1,596 men with pleural plaques fulfilling strict radiologic criteria were identified from 1963 until June 1985. The men have been followed prospectively for 16,369 person-years. The number of mesotheliomas and bronchial carcinomas was compared with the age- and year-specific expected incidence from the official cancer registry of Sweden. Fifty bronchial carcinomas occurred, while 32.1 were expected after correction for smoking habits, a difference which was statistically significant. Patients with radiologic asbestosis were overrepresented among those with bronchial carcinoma. The risk for patients with pleural plaques without asbestosis was increased 1.4 times, which was statistically significant. There were 9 mesotheliomas, while only 0.8 were expected. The mean latency time from first exposure to diagnosis of bronchial cancer was 44.1 years and for mesothelioma was 48.1 years. Thus, pleural plaques on the chest roentgenogram indicate significant exposure to asbestos, with an increased risk for mesothelioma and possibly also for bronchial carcinoma. Any person found to have plaques on chest roentgenogram should be informed of them and should be persuaded to stop smoking.