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PubMed1988

Asbestos-contaminated drinking water: its impact on household air.

Asbestos contamination in excess of 10 billion fibers per liter was detected in a community's drinking water. To assess the possibility of waterborne asbestos becoming airborne, air samples were collected from impacted houses receiving contaminated water from three control houses. Collected within each house were three samples on 0.6-micrometer-pore Nuclepore filters and three samples on 0.8-micrometer-pore Millipore filters. In addition, bulk samples of suspect material and water samples were collected. Mean waterborne asbestos concentrations were 24 million fibers per liter (MFL) in the impacted houses versus only 1.1 MFL in the control houses. Transmission electron microscopy revealed that airborne asbestos concentrations were highest in impacted houses, with airborne asbestos concentrations positively correlated with waterborne concentrations. For fiber and mass measurements on both filter types, airborne asbestos concentrations were significantly higher in the impacted houses: mean concentrations in impacted houses were 0.12 fibers/cm3 and 1.7 ng/m3 on Nuclepore filters and 0.053 fibers/cm3 and 2.3 ng/m3 on Millipore filters versus only 0.037 fibers/cm3 and 0.31 ng/m3 on Nuclepore filters and 0.0077 fibers/cm3 and 0.14 ng/m3 on Millipore filters from control houses. Also detected in the air samples from impacted houses were clusters of chrysotile, often with several hundreds of fibers. When estimates of these individual fibers were added to the total fiber count, the difference between the impacted and control houses became even greater. The increased concentrations in impacted houses were due primarily to short (less than 1 micrometer) fibers. Bulk samples did not reveal likely materials within the impacted houses to account for these differences. Thus high levels of waterborne asbestos were apparently the source of increased concentrations of airborne asbestos within these houses.

Air Pollutants↗

PubMed1984

Morphology of small-airway lesions in patients with asbestos exposure.

The morphologic changes in the small airways of 15 patients who had been exposed to asbestos and had abnormalities of the respiratory bronchioles and alveolar ducts were examined and compared with changes in the small airways of a matched group of cigarette smokers. Lesions were evaluated using a visual grading scheme to determine pathologic severity of fibrosis, inflammation, and pigmentation in these airways. The membranous bronchioles of both asbestos-exposed and cigarette exposed patients showed the deposition of fibrous tissue and pigment; the lesions were morphologically identical, although more severe in the asbestos group (67 per cent of airways) than in the smoking group (19 per cent of airways). A distinctive lesion, consisting of fibrosis often accompanied by pigment, was found in 74 per cent of the respiratory bronchioles in the asbestos-exposed patients, compared with 6 per cent of respiratory bronchioles in the smokers. Similar changes were found in 49 per cent of alveolar ducts in the asbestos group and 1 per cent of the ducts in smoking group. Asbestos bodies were found in only 11 of 15 cases. The authors conclude that a distinctive lesion of small airways exists in some asbestos workers and that it can be identified by the finding of marked fibrosis in the walls of respiratory bronchioles and alveolar ducts. Because there is no proof that this lesion actually progresses to interstitial fibrosis (asbestosis), the authors suggest that it be termed "asbestos airways disease."

Asbestos↗

PubMed1981

The need to control asbestos fibers in potable water supply systems.

Occupational studies have shown that asbestos is a human carcinogen. Because many inhaled asbestos fibers deposited in the lung are cleared and swallowed, workers are also exposed through ingestion. Of the millions of current and former workers who have been heavily exposed to asbestos, one in ten will die from cancer of the gastrointestinal tract. A number on the order of 1 in 1,000 ingested asbestos fibers penetrate the digestive tract and ingested fibers have been recovered in such tissues as kidney, intestine, liver, and urine. One animal study showed tumor production related to ingestion of asbestos-containing material but, in general, the results of seven animal feeding studies have been inconclusive. A statistically significant relationship between male lung and stomach cancer and female peritoneal, gall bladder, and esophageal cancer and asbestos counts in drinking water was determined in one epidemiology study. Increased rates for male stomach and lung, and female pancreatic cancer related to asbestos in drinking water were reported in another study but possible occupational exposure made it difficult to draw conclusions. Data on excess gastrointestinal cancer among occupational groups has been used to estimate that drinking water containing 300,000 asbestos fibers per liter over a lifetime will result in one additional cancer among 100,000 people.

Asbestos↗

PubMed2001

Asbestos fiber burdens in lung tissues of Hong Kong Chinese with and without lung cancer.

To investigate the asbestos exposure level in non-occupational population and its relation to lung cancer, pulmonary asbestos fiber counts were observed with a modified alkali digestion method, in lung tissues from 65 random surgically treated lung cancer patients (42 males and 23 females) and that obtained from 107 random autopsy cases who died of either accidental death or acute myocardial infarction (44 males and 63 females) during 1987-1988. The patients and cases were all Hong Kong Chinese with no definite history of occupational exposure to asbestos. The non-lung cancer cases (NLCC) were divided into three groups based on different age ranges: 10 approximately, 40 approximately and 70 approximately years. The results showed that the medians of uncoated fiber counts (0, 32 and 52 fibers per mg dry tissue [f/mgDT] in the different age groups, respectively) increased in an age-dependent manner (P<0.01). However, the medians of coated fiber (asbestos body) counts were all 0 f/mgDT, with no statistically significant difference among the groups, showing a very low level of asbestos body burden in NLCC. In each age group, no difference in those counts between males and females was observed (P>0.05). Moreover, those counts in male lung cancer cases (medians of 62.5 and 17.5 f/mgDT, respectively) were greater than that in the control (32.5 and 0 f/mgDT, respectively) (P<0.01, P<0.05, respectively), however, regarding the female groups there was no statistically significant difference from the control. The results suggest that there is an environmental exposure to asbestos in Hong Kong Chinese, the level of which is, however, generally not sufficient to induce asbestos body. Environmental asbestos exposure in Hong Kong males may be one of the carcinogenic factors leading to lung cancer.

Accidents↗

PubMed1998

Asbestos-induced pleural disease.

Asbestos-induced pleural disease has become the most common manifestation of asbestos exposure. Asbestos has an unusual affinity for the pleural space and leads to plaques, benign effusions, fibrosis, and malignant mesothelioma. The explanation for its affinity for the pleura may lie in part with new evidence showing that asbestos fibers can accumulate in certain regions of the parietal pleura at higher concentrations than in the lung. With the control of industrial exposures to asbestos, the incidence of this disease should decrease, with the incidence of mesothelioma peaking in the years 2000 to 2020. Nonetheless, the toxic features of asbestos including shape, chemical composition, and surface characteristics should be understood to avoid toxicity in fibers used to replace asbestos and to know the risks of low level exposures from asbestos currently in our environment.

Asbestos↗

PubMed1999

Environmental asbestos exposure and malignant pleural mesothelioma.

Asbestos-related benign and malignant pleural diseases are endemic in some rural parts of central Turkey because of environmental exposure to asbestos fibres. We report here epidemiological data on 113 patients with diffuse malignant pleural mesothelioma (DMPM) diagnosed in our clinic in Eskişehir, located in central Turkey. Of the 113 patients, 59 were men and 54 women (male:female ratio = 1). Ninety-seven patients (86%) had non-occupational asbestos exposure; all were living in villages. Their mean age was 56 years. As the patients had been exposed to asbestos from birth, the latency period was equivalent to the age of the patients. Twenty-eight patients (29%) had lived in villages their entire lives. The other 69 (71%) had been born in a village but migrated to the city or had given up white-soil usage for various reasons. The mean exposure time was 55 years for those with a long exposure period and 25 years for those with a short exposure period, but there was no significant difference between the age of the disease appearance for both groups (55 and 56 years, respectively). Thus, the latency time of mesothelioma due to environmental exposure to asbestos was longer than that due to occupational exposure, but independent of the length of exposure. Soil samples from 67 villages were analysed, comprising a population of 10,120 villagers. Tremolite and some other types of asbestos were found. In conclusion, DMPM in our region is due to mainly to environmental exposure to asbestos. The risk is substantial as a large proportion of the villagers are exposed. After smoking, asbestos exposure is one of the most serious health hazards in our rural population.

Adult↗

PubMed2002

Diseases caused by asbestos: mechanisms of injury and disease development.

Asbestos is a ubiquitous, naturally occurring fiber that has been linked to the development of malignant and fibrotic diseases of the lung and pleura. These diseases may be initiated by injury to epithelial cells and mesothelial cells by asbestos fibers through the formation of reactive oxygen intermediates. Elaboration of oxidants are also a consequence of inflammation, a hallmark of exposure to asbestos after inhalation or injection of asbestos fibers into animals. The type, size, and durability of asbestos fibers may be important in toxicity and pathogenicity of asbestos types. This review discusses the pathways of oxidant generation by asbestos fibers, cell-cell interaction that may initiate and perpetuate inflammation, cytokine release and proliferative responses to asbestos, and cell signaling pathways implicated in these events.

Animals↗

PubMed1998

Development of a method for the determination of low contents of asbestos fibres in bulk material.

Asbestos is a category 1 carcinogen under the EU classification, but in the absence of a method to quantify asbestos in a matrix at the 0.1% level, there has been a delay in implementing relevant directives to asbestos. An analytical scheme for identification and quantification of asbestos using polarised light microscopy (PLM) and phase contrast optical microscopy (PCM) has now been developed. When used on artificial mixtures by an experienced laboratory, it achieved the required target performance, at 0.1% asbestos concentration by mass in a bulk sample, to obtain a result, which with 90% probability, is correct within a factor of two. The method of identification by PLM and quantification by PCM has been assessed by interlaboratory comparisons. The method begins with an initial identification using PLM, and depending on asbestos type and matrix a combination of preparation procedures are used to produce the analytical filter. A gentle comminution method was used which reduces the risk of overmilling. The asbestos mass percentage on the filter is quantified using PCM in combination with a PLM attachment for identification of possible non-asbestos fibres. The final method is supported by efficient methods for fibre identification for size determination and calculation of total fibre volume. A statistical analysis of mass concentration estimates was made and the effect of preferred orientation of fibres on the analytical filter was quantified.

Asbestos↗

PubMed2006

Crocidolite asbestos and SV40 are cocarcinogens in human mesothelial cells and in causing mesothelioma in hamsters.

Only a fraction of subjects exposed to asbestos develop malignant mesothelioma (MM), suggesting that additional factors may render some individuals more susceptible. We tested the hypothesis that asbestos and Simian virus (SV40) are cocarcinogens. Asbestos and SV40 in combination had a costimulatory effect in inducing ERK1/2 phosphorylation and activator protein-1 (AP-1) activity in both primary Syrian hamster mesothelial cells (SHM) and primary human mesothelial cells (HM). Ap-1 activity caused the expression and activation of matrix metalloprotease (MMP)-1 and MMP-9, which in turn led to cell invasion. Experiments using siRNA and chemical inhibitors confirmed the specificity of these results. The same effects were observed in HM and SHM. Experiments in hamsters showed strong cocarcinogenesis between asbestos and SV40: SV40 did not cause MM, asbestos caused MM in 20% of hamsters, and asbestos and SV40 together caused MM in 90% of hamsters. Significantly lower amounts of asbestos were sufficient to cause MM in animals infected with SV40. Our results indicate that mineral fibers and viruses can be cocarcinogens and suggest that lower amounts of asbestos may be sufficient to cause MM in individuals infected with SV40.

Animals↗

PubMedDate not supplied

High prevalence of reversible airway obstruction in asbestos-exposed workers.

In this retrospective study of 97 male workers exposed to asbestos for 2-50 yr, data were collected on chest x-ray findings and lung function, including lung volumes, forced expiratory flow rates (i.e., forced expiratory volume in 1 sec [FEV1.0], forced expiratory flow measured between 25% and 75% of forced vital capacity [FEF(25-75%)]), airway resistance (R(aw)), carbon monoxide (CO)-diffusing capacity, and the existence of airway obstruction reversible by a beta-adrenergic agonist (RAO). The authors performed multiple-regression analyses to correlate the variations in lung function data with age, smoking habits, duration of asbestos exposure, and time since last exposure. Occupational activities of subjects that might induce specific lung abnormalities were also considered. No significant decrease was seen in lung volumes or CO-diffusing capacity; however, a decrease in FEV1.0 and an increase in R(aw) were measured in 65% of the subjects, and an isolated decrease in FEF(25-75%) occurred in only 18%. There was no difference in lung-function data between subjects who had chest x-ray signs of abnormalities (n = 59) and those who did not (n = 38). A significant relationship was found between the decrease in FEV1.0 and age; however, no correlation was noted between altered lung function and cigarette smoking, duration of asbestos exposure, or time since last exposure. RAO prevalence was higher (34%) than previously reported (9%) in subjects with chronic obstructive pulmonary disease (COPD) who were not exposed to asbestos or outdoor pollution. The RAO prevalence in asbestos-exposed workers was nearly the same as that measured in COPD subjects who lived downtown and who were exposed to outdoor pollution (36%). The high RAO prevalence in asbestos-exposed workers was found in 43% of subjects who were exposed only to asbestos, and in 33% of subjects who were also exposed to air pollution due to their occupational activities. It is hoped that the observations in this study will encourage practitioners to check for RAO in asbestos workers who use inhaled bronchodilators.

Aged↗

PubMed2006

Conference summary. Directions and needs in asbestos research: new insights.

The Center for Environmental Health Sciences (CEHS) Conference entitled "Directions and Needs in Asbestos Research: New Insights" was held at the University of Montana in Missoula on July 28 and 29, 2005. Researchers, physicians, health care workers, and federal agency representatives from around the country met for a cross-disciplinary exploration of many issues related to asbestos research. Topics included community and psychosocial issues in biomedical research, asbestos exposure assessment, assessment and mechanisms of asbestos-related diseases, and new research directions. This meeting report is a summary of the conference presentations, and of the topics identified for future research directions. This conference was a follow-up to one hosted by the CEHS in June 2002, and continued to take advantage of opportunities to work with a unique population in Libby, MT, where significant asbestos exposures have occurred due to the mining of asbestos-contaminated vermiculite. The goals of this conference were to bring together experts from diverse fields to identify progress made since the last conference and to develop new research avenues that would allow us to address the research needs in emerging asbestos-exposed populations. Participants indicated that these objectives were met, and expressed enthusiasm for follow-up conferences, tentatively planned for the summer of 2007, to maintain the dialog that has been established regarding directions and needs in asbestos research. Selected papers from the conference are presented in this issue of Inhalation Toxicology.

Asbestos↗

PubMed2006

Evidence and reconstruction of airborne asbestos from unconventional environmental samples.

The understanding of historical ambient asbestos concentrations is critical to exposure mapping and retrospective health impact studies involving asbestos related diseases. Two presentations at the University of Montana Center for Environmental Health Sciences Asbestos Conference (July 28, 2005) introduced novel methods for detecting evidence of past airborne asbestos contamination. In each of these studies, transmission electron microscopy was used to identify and measure asbestos fibers collected in samples from unconventional environmental sources. In the first study, paleolimnology, analytical transmission electron microscopy, particle-separation techniques, and empirical aerosol-sediment modeling were combined to provide the first measurements of airborne asbestos concentrations prior to the 1980s. In an upstate New York study area, airborne concentrations of chrysotile followed its 20th-century usage, with highest concentrations near mid-century (approximately 0.1 fibers/cm3), followed by a decrease in the last quarter century. Airborne concentrations of anthophyllite asbestos (a contaminant from nearby talc mines and mills) increased from <0.004 to 0.022 fibers/cm3 from 1847 to 1995. In the second study, tree bark and core samples were collected from areas near the asbestos-contaminated vermiculite mine in Libby, MT. We originally hypothesized that trees in the areas surrounding the mine could serve as reservoirs for ambient amphibole fibers. Though gravimetric reduction of a tree core sample did not indicate the presence of amphibole fibers, transmission electron microscopy analysis of bark samples yielded substantial amphibole fiber concentrations ranging from 14 to 260 million amphibole fibers/cm2. Based on these preliminary results, we conclude that trees in the Libby valley can serve as reservoirs for amphibole fibers, and that a continued potential for exposure exists for those who harvest contaminated wood.

Air Pollutants↗

PubMed2002

Impact of asbestos concentrations in floor tiles on exposure during removal.

This study investigated personal airborne exposure to asbestos during its abatement in two projects that had floor tile with different concentrations of asbestos. Abatement of floor tile with the higher percent asbestos exhibited the highest personal exposure level. Airborne exposure concentrations of asbestos between these abatement projects were found to be statistically significant. However, since neither had levels above occupational exposure standards this difference was not considered important, a type two error (false positive). It is suggested that when establishing negative exposure assessments, priority be given to process/work practices, with percent of contaminant in the building component being of less importance. Time period of applicability of data from negative exposure assessments to future projects should be considered indefinite. Neither within- or between-worker variation was predominant, in this study. Likelihood of exceeding occupational exposure standards during abatement of asbestos-containing floor tile, even for materials containing up to 15% asbestos, is low. Regulation of floor tile as a special category or group of asbestos-containing material appears to be warranted. Current schemes in the United States that regulate floor tile in the same group as other asbestos-containing materials would appear to be a legislating of science.

Air Pollutants, Occupational↗

PubMed2001

Cancer mortality among workers exposed to amphibole-free chrysotile asbestos.

The issue of whether exposure to chrysotile asbestos alone, without contamination from amphibole asbestos, causes lung cancer and mesothelioma was investigated in a 25-year longitudinal study (1972-1996) in Chongqin, China. The study cohort comprised 515 male asbestos plant workers exposed to chrysotile only; the control cohort included 650 non-dust-exposed workers. The results of analysis in which the proportional hazards model was used indicated that mortality due to all causes, all cancers, and lung cancer was related to asbestos exposure; the relative risks, adjusted for age and smoking, were 2.9, 4.3, and 6.6, respectively. Fiber concentrations in the raw material section and the textile section of the plant were 7.6 and 4.5 fibers/ml, respectively. Because of differences between the study and control plants, the authors also compared various sections of the asbestos plant that had different levels of dust exposure. The adjusted relative risk of lung cancer was 8.1 for workers exposed to high versus low levels of asbestos. Two cases of malignant mesothelioma, one pleural and the other peritoneal, were found in the asbestos cohort. These results suggest that heavy exposure to pure chrysotile asbestos alone, with negligible amphibole contamination, can cause lung cancer and malignant mesothelioma in exposed workers.

Age Factors↗

PubMed1999

Asbestos related mortality in Northern Ireland: 1985-1994.

BACKGROUND: The association between Belfast and research into the hazardous effects of asbestos exposure goes back many years. This paper aims to update previous papers and review the burden of asbestos related disease in Northern Ireland today. METHODS: A study was carried out of all deaths in Northern Ireland between 1985 and 1994 inclusive, in which an asbestos related disease was mentioned anywhere on the death certificate. RESULTS: During this 10 year period, 527 asbestos related deaths were recorded; 88 per cent of these were in men. A total of 410 (77.8 per cent) were registered as the primary cause of death but only 405 (76.9 per cent) of cases were the subject of an autopsy. Standardized rates of pleural cancer in males have been increasing at 3.2 per cent per year though the trend was not significant. Lower rates in the last two years may herald the commencement of a decline. Deaths were clustered around the Belfast estuary, the site of Northern Ireland's shipbuilding industry. High proportional mortality ratios were demonstrated for occupations associated with the shipbuilding and construction industries. Evidence is presented that casts doubt on the attribution of peritoneal cancers in females to asbestos exposure. If lung cancers are included, there may be an average of 81 asbestos related deaths in Northern Ireland every year. CONCLUSION: Asbestos related diseases continue to extract a heavy burden of ill health in Northern Ireland today. There are some indications that the upward trend may be on the wane but confirmation of this will have to await further data. Measures to reduce exposure in the workplace to both asbestos and to tobacco smoke are the only means of reducing this burden.

Aged↗

PubMed2000

Identifying industrial sites with potential for residential exposure to asbestos.

BACKGROUND: Non-occupational exposure to asbestos has been of increasing interest, but residential exposure to asbestos often focuses on a few high-profile asbestos users. This study aimed to identify industrial sites producing asbestos goods in a given area and time period. METHODS: A search of trade directories was carried out for industrial sites in West Yorkshire, England, where asbestos may have been used this century. RESULTS: A large number of factories with potential for residential exposure were found. A total of 269 factories in West Yorkshire used asbestos between 1900 and 1979, many for short periods only. CONCLUSIONS: Identification of potential sources of residential exposure to asbestos would have greatly underestimated their number if either only high-profile users or existing official listings had been used. Any consideration of asbestos use should aim to identify all users, not just the high-profile manufacturers.

Asbestos↗

PubMed1979

Radiographic search for asbestos-related disease in a naval shipyard.

The Long Beach Shipyard underwent a chest x-ray survey of 6640 employees, or 88.6% of the total shipyard population, to determine the level of asbestotic changes. For computer classification purposes, the findings were divided into five groups: abnormal findings consistent with inhalation of asbestos fiber; normal; pulmonary fibrosis, nonspecific, questionable; and other findings not related to asbestosis. Asbestos-related abnormal findings, were encountered in 1061 workers, or 16.0%. No change was noted in 4806, or 72.4%. Pulmonary fibrosis was encountered in 140, or 2.1%. Other abnormalities not related to the inhalation of free asbestos fiber were encountered in 624, or 9.4%. The interpretation was questionable in nine individuals, or 0.1%. Of the male employees, 17.2% were positive for asbestos-related chest x-ray changes, and four women, or 0.8%, showed comparable findings. Of the men, 71.5% had normal chest x-rays, and 83.3% of the 402 women demonstrated normal films. Positive x-ray changes for asbestosis were encountered in a linear relationship when viewed by age of the worker. Employees aged 25--29 years exhibited 1.3% positive findings, and this level increased to a maximum of 38.2% positives among workers aged 65 years and over. Normal chest films descended, conversely, in a linear relationship. Similarly, the percentage of positive findings for asbestos-related disease increased in a linear configuration with length of service. Persons with 2--6 years of asbestos contact displayed 12.4% positive findings, while individuals with 22-26 years of work at the shipyard manifested 37.0% positive chest film findings. Although the shipyard was operational between 1943 and 1949, the system of allocation of badge numbers precludes the inclusion of these 7 years of work among persons who had had at least 26 years of service. When studied by work site, dividing the subjects into production and nonproduction personnel, it was found that production workers accounted for 74.5% of the asbestos-positive films. Overall, the 780 production workers manifested 11.8% of the positive findings of all persons studied, while nonproduction employees accounted for 4.1% of the positives out of the population studied. A figure that approximates the total finding of asbestos-related disease is 16.0%.

Adult↗

PubMed1979

Levels of asbestos air pollution in some environmental situations.

Asbestos contamination of the outside aid in Paris and suburbs has been monitored in some environmental situations, namely, "typical" urban sites removed from known sources of asbestos emissions, crossroad locations, the vicinity of a freeway, areas with buildings under construction, and areas around asbestos factories. In the same manner, measurements have been performed inside buildings of various types: those sprayed with asbestos-containing materials, those fitted with asbestos products, and control buildings. Air has been sampled by use of 0.45 micrometer pore size Millipore filters. After low-temperature ashing, ultrasonicated ashes were transferred to carbon film on 200-mesh gold grids examined under an analytic transmission electron microscope. Levels of pollution were expressed in terms of gravimetric concentrations. Inside buildings, when the air was in contact with significant amounts of asbestos-containing materials (spray, sheets), the levels were in the range 0.1--1000 10(-9) g m-3. In the vicinities of asbestos plants, the concentrations were higher: 1000--3000 10(-9) g m-3. Under other circumstances, the levels were of the same order of magnitude: 99% of the values were below 7 X 10(-9) g m-3. The Conseil Supérieur d'Hygiène Publique de France proposed a numerical ambient air quality standard of 50 X 10(-9) g m-3 inside buildings sprayed with asbestos.

Air Pollutants↗