Electricians’ chrysotile asbestos exposure from electrical products and risks of mesothelioma and lung cancer

Both mechanistic and epidemiology studies indicate chrysotile asbestos has a threshold below which it does not cause mesothelioma or lung cancer. We conducted a critical review to determine whether electricians are at increased risk for these cancers and, if so, whether their exposure to chrysotile in electrical products could be responsible. We found that most, but not all, epidemiology studies indicate electricians are at increased risk for both cancers. Studies that evaluated electricians’ exposure to asbestos during normal work tasks have generally reported low concentrations in air; an experimental study showed that grinding or drilling products containing encapsulated chrysotile resulted in exposures to chrysotile fibers far below the OSHA permissible exposure limit and the cancer no observed adverse effect level. Studies of other craftsmen who often work in the vicinity of electricians, such as insulators, reported asbestos (including amphibole) exposures that were relatively high. Overall, the evidence does not indicate that exposure to chrysotile in electrical products causes mesothelioma or lung cancer in electricians. Rather, the most likely cause of lung cancer in electricians is smoking, and the most likely cause of mesothelioma is exposure to amphibole asbestos as a result of renovation/demolition work or working in the proximity of other skilled craftsmen.     

Oncolyn对温石棉所致大鼠氧化损伤影响的实验研究

目的探讨温石棉对实验大鼠氧化损伤的影响以及Oncolyn的缓解作用。方法Wistar大鼠随机分为对照组、石棉组和Oncolyn组,应用支气管灌注的方法给予大鼠温石棉5mg/ml,同时经口给入Oncolyn40d,剂量为1.5g/(kg·d),检测肺泡巨噬细胞中DNA损伤状况以及血液和肺脏中NO、NOS和抗氧化酶SOD、CAT、GSHPx、GST的活性。结果石棉组肺泡巨噬细胞DNA链断裂增加,表现为彗星出现率和DNA迁移长度增加;血液中NO和NOS水平和SOD、GSHPx活性增加,而GST活性下降;而肺组织中NOS、SOD、GSHPx和GST的活性均下降,MDA含量增加。应用Oncolyn预防后,肺泡巨噬细胞DNA损伤下降;血液中NO、NOS的水平以及SOD活性下降,而GSHPx、GST、CAT活性上升;肺组织中抗氧化酶活性增加,MDA含量下降。结论Oncolyn对温石棉所致机体氧化损伤有一定的缓解作用。     

The health effects of chrysotile: current perspective based upon recent data

This review substantiates kinetically and pathologically the differences between chrysotile and amphiboles. The serpentine chrysotile is a thin walled sheet silicate while the amphiboles are double-chain silicates. These different chemistries result in chrysotile clearing very rapidly from the lung (T(1/2)=0.3 to 11 days) while amphiboles are among the slowest clearing fibers known (T(1/2)=500 days to infinity). Across the range of mineral fiber solubilities chrysotile lies towards the soluble end of the scale. Chronic inhalation toxicity studies with chrysotile in animals have unfortunately been performed at very high exposure concentrations resulting in lung overload. Consequently their relevance to human exposures is extremely limited. Chrysotile following subchronic inhalation at a mean exposure of 76 fibers L>20 microm/cm(3) (3413 total fibers/cm(3)) resulted in no fibrosis (Wagner score 1.8-2.6), at any time point and no difference with controls in BrdU response or biochemical and cellular parameters. The long chrysotile fibers were observed to break apart into small particles and smaller fibers. Toxicologically, chrysotile which rapidly falls apart in the lung behaves more like non-fibrous mineral dusts while response to amphibole asbestos reflects its insoluble fibrous structure. Recent quantitative reviews of epidemiological studies of mineral fibers have determined the potency of chrysotile and amphibole asbestos for causing lung cancer and mesothelioma in relation to fiber type have also differentiated between these two minerals. The most recent analyses also concluded that it is the longer, thinner fibers that have the greatest potency as has been reported in animal inhalation toxicology studies. However, one of the major difficulties in interpreting these studies is that the original exposure estimates rarely differentiated between chrysotile and amphiboles. Not unlike some other respirable particulates, to which humans are, or have been heavily occupationally exposed, there is evidence that heavy and prolonged exposure to chrysotile can produce lung cancer. The value of the present and other similar studies is that they show that low exposures to pure chrysotile do not present a detectable risk to health. Since total dose over time decides the likelihood of disease occurrence and progression, they also suggest that the risk of an adverse outcome may be low if even any high exposures experienced were of short duration.     

Quantification of the pathological response and fate in the lung and pleura of chrysotile in combination with fine particles compared to amosite-asbestos following short-term inhalation exposure

The marked difference in biopersistence and pathological response between chrysotile and amphibole asbestos has been well documented. This study is unique in that it has examined a commercial chrysotile product that was used as a joint compound. The pathological response was quantified in the lung and translocation of fibers to and pathological response in the pleural cavity determined. This paper presents the final results from the study. Rats were exposed by inhalation 6?h/day for 5 days to a well-defined fiber aerosol. Subgroups were examined through 1 year. The translocation to and pathological response in the pleura was examined by scanning electron microscopy and confocal microscopy (CM) using noninvasive methods. The number and size of fibers was quantified using transmission electron microscopy and CM. This is the first study to use such techniques to characterize fiber translocation to and the response of the pleural cavity. Amosite fibers were found to remain partly or fully imbedded in the interstitial space through 1 year and quickly produced granulomas (0 days) and interstitial fibrosis (28 days). Amosite fibers were observed penetrating the visceral pleural wall and were found on the parietal pleural within 7 days postexposure with a concomitant inflammatory response seen by 14 days. Pleural fibrin deposition, fibrosis, and adhesions were observed, similar to that reported in humans in response to amphibole asbestos. No cellular or inflammatory response was observed in the lung or the pleural cavity in response to the chrysotile and sanded particles (CSP) exposure. These results provide confirmation of the important differences between CSP and amphibole asbestos.     

Chrysotile as a Cause of Mesothelioma: An Assessment Based on Epidemiology

There has been a longstanding debate about the potential contribution of chrysotile asbestos fibers to mesothelioma risk. The failure to resolve this debate has hampered decisive risk communication in the aftermath of the collapse of the World Trade Center towers and has influenced judgments about bans on asbestos use. A firm understanding of any health risks associated with natural chrysotile fibers is crucial for regulatory policy and future risk assessments of synthesized nanomaterials. Although epidemiological studies have confirmed amphibole asbestos fibers as a cause of mesothelioma, the link with chrysotile remains unsettled. An extensive review of the epidemiological cohort studies was undertaken to evaluate the extent of the evidence related to free chrysotile fibers, with particular attention to confounding by other fiber types, job exposure concentrations, and consistency of findings. The review of 71 asbestos cohorts exposed to free asbestos fibers does not support the hypothesis that chrysotile, uncontaminated by amphibolic substances, causes mesothelioma. Today, decisions about risk of chrysotile for mesothelioma in most regulatory contexts reflect public policies, not the application of the scientific method as applied to epidemiological cohort studies.     

Effectiveness of serum megakaryocyte potentiating factor in evaluating the effects of chrysotile and its heated products on respiratory organs

Chrysotile (CH), the most common form of asbestos, is rendered less toxic by heating it at 1000 °C and converting it to forsterite (FO-1000). However, further safety tests are needed to evaluate human health risk of these materials. It has been reported that serum concentrations of megakaryocyte potentiating factor N-ERC/mesothelin become elevated in patients with mesotheliomas caused by asbestos exposure. In this study, a single 2 mg dose of CH or FO-1000 was intratracheally administered to rats. Within 180 days after the administrations, serum N-ERC/mesothelin concentrations, levels of 8-hydroxy-2'-deoxyguanosine (8-OHdG) in lung tissues and pathological changes in respiratory organs were determined. In the CH group, a significant increase in serum N-ERC/mesothelin concentrations was observed immediately after intratracheal administration, and the elevation lasted for 30 days. In lung tissues, positive staining for 8-OHdG in bronchioles, alveolar epithelium, inflammatory cells, and granulomas was evidence of a marked DNA oxidative damage. Furthermore, measurements of 8-OHdG in lung tissues based on the HPLC-ECD method suggested that serum N-ERC/mesothelin concentrations tended to increase when there are significant DNA damages in lung tissues. In contrast, in the FO-1000 group, a marked rise in serum N-ERC/mesothelin concentrations occurred only in the early phase (1-7 days) after intratracheal administration. Similarly, FO-1000 induced elevation of 8-OHdG in lung tissues was transient and modest compared with those of the CH-treated animals. In both the CH and FO-1000 groups, we observed significant correlations between serum N-ERC/mesothelin concentrations and lung 8-OHdG concentrations (r = 0.559, p = 0.001 for the CH group; r = 0.516, p = 0.01 for the FO-1000 group). In summary, we demonstrated the possibility of using serum N-ERC/mesothelin concentrations as a useful biomarker for early phase exposure to either CH or FO-1000.     

Cancer mortality among Chinese chrysotile asbestos textile workers

To determine mortality associated with exposure to chrysotile asbestos, a cohort of asbestos workers from an asbestos textile factory in China was followed prospectively from 1972 to 2008. A total 577 workers were successfully followed, achieving a follow-up rate of 98.5% over 37 years. Employment data and smoking information were obtained from factory and individual workers. Vital status was ascertained from factory personnel records and the municipal death registry. Workers were categorized into high, medium and low exposure groups in terms of their job titles and workshops. Follow-up generated 17,508 person-years, with 259 deaths from all causes, 96 all cancers and 53 lung cancers and 2 mesotheliomas. The highest cancer mortality was observed in the high exposure group, with 1.5-fold age-adjusted mortality from all cancers and 2-fold from lung cancer compared to the low exposure group. Age and smoking adjusted hazard ratio in the high exposure group was 2.99 (95%CI, 1.30, 6.91) for lung cancer and 2.04 (1.12, 3.71) for all cancers. Both smokers and nonsmokers at the high exposure level had a high death risk of lung cancer, with a clearer exposure-response trend seen in smokers. This study confirmed increased mortality from lung cancer and all cancers in asbestos workers, and the cancer mortality was associated with exposure level.     

Assessing specific causation of mesothelioma following exposure to chrysotile asbestos-containing brake dust

Abstract

Background: The question of whether chrysotile asbestos-containing brake dust can plausibly serve as a cause of mesothelioma in an exposed individual has become a matter of heated debate in the medical literature despite multiple international, federal, and state governmental agencies acknowledging a causal association.

Objectives: We describe and provide an analysis of various industry and academic perspectives contributing to the debate.

Methods: A framework is presented for evaluating the general and specific causal relationship between brake dust exposure and mesothelioma utilizing the principles of forensic epidemiology, and by applying the Bradford–Hill criteria.

Results and conclusions: We conclude that there is a “net” of evidence favoring a causal relationship between brake dust-associated chrysotile exposure and mesothelioma. The industry-sponsored position that there is insufficient evidence to support a contiguous “chain” of causation is specious from both a methodologic and evidentiary perspective. Finally, we suggest a semiquantitative approach for the evaluation of individual causation in putative cases of mesothelioma with a history of significant brake dust exposure.     

Mesothelioma associated with use of drywall joint compound: a case series and review of literature

Abstract

Background: Drywall joint compound contained asbestos fibers, primarily chrysotile, in the 1950s through the 1970s. Workers in a variety of construction trades and homeowners were exposed to respirable asbestos from the use of these products, including during handling, mixing, sanding, and sweeping. Disturbance of in-place asbesto-containing joint compound continues to be a potential source of exposure during demolition or repair of wallboard. Studies from the 1970s and 1980s report air fiber measurements above current and historic regulatory limits during intended usage, and typical asbestos-related disease in drywall construction workers.

Objectives: We present three cases of mesothelioma in which the only known exposure to asbestos was from joint compound and review the literature on exposure circumstances, dose and fiber types.

Conclusions: Physicians treating mesothelioma patients should obtain a history of exposure to these products during work or home remodeling.