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This page is written in 2006, from a Canadian perspective, and is based on legislation in Quebec. It was reviewed in 2021 by Edouard Bastarache, he noted the following (which we updated in the text):
We got a detailed report from the North American Insulation Manufacturers Association (“NAIMA”) Apr 2021, see the link below to read it also.
This text deals with the freshly-manufactured product. But it does not consider the effect of repeated heat/cool cycles that products may experience in service. Do those cycles transform the fibres from amorphous to crystalline? What physical property changes and new hazards accompany that transformation?
Man-made vitreous fibers (MMVF) or synthetic vitreous fibers (SVFs) are a class of insulating materials used widely in residential and industrial settings; they are made primarily from glass, rock, slag or clay. The three general categories are fiberglass, mineral wool , and refractory ceramic fibers.
In some situations, SVF materials can release fine, airborne dust particles, some of which are small enough to be respirable. Thus, workers may be exposed to SVF fibers by dermal contact and/or by inhalation.
Fibrous particles having long, thin geometry present a special problem to the resiratory tract; because fibers are thin, they can penetrate into the deep lung and, because they are long, mobile lung cells may have difficulty in removing them.
A. Fiber Glass
B. Mineral Wool
C. Refactory Ceramic Fibers (RCFs)
SVFs can help to control heat flow, absorb acoustic energy, filter impurities from gases and liquids, and with a vapor barrier, control condensation.
An important attribute of these fibers is that they do not split longitudinally as do asbestos fibers. Because asbestos fibers tend to split longitudinally, over time in the lung, the number of lung, thin asbestos fibers can actually increase, resulting in increasing lung irritation even after exposure to asbestos has stopped.
In contrast, SVFs tend to break tranversely into shorter segments, which the lung can clear more readily than it can long fibers.
Fiberglass is produced in two basic forms, wool fibers and textile fibers.
Mineral wools include rock or stone wool and slag wool. After formation, the materials are sprayed with lubricating oils and binders to reduce dustiness (mineral wools generally contain a very high ratio of nonfibrous particles, or shot) and fiber breakage. Mineral wool applications are very similar to those of glass wool-thermal insulation, including fire protection, and acoustic insulation. Much of the mineral wool produced is used for blown-in insulation in attics and side walls. Another popular use of mineral wool is in the manufacture of decorative and acoustic ceiling tiles for commercial building.
Refractory ceramic fiber (RCF) is formulated to help control heat flow in high-temperature, industrial situations. All RCFs are blends of alumina and silica and other refractory oxides.
The three general categories of RCFs are:
Applications vary for RCFs, but all are used in high-temperature, industrial environments.
RCF blankets are used as furnace and kiln liners, as backup insulation to refractory brick, as soaking pit covers, and in annealing welds. Loose RCF is used as a filler in packing voids and in expansion joints. Custom-molded shapes of RCF are used widely in metal molding, in catalytic converters, and as combustion chamber liners in industrial furnaces.
SVFs may irritate the skin of some workers who are engaged in manufacturing, fabricating, or installing SVF products. This irritation is a mechanical reaction to sharp, broken ends of fibers that rub or become embedded in the outer layer of the skin and does not appear to be an allergic response. Typically, irritation does not persist and can be relieved by washing exposed skin gently with warm water and mild soap.
If large amounts of airborne fine fiber are released during manufacturing or handling of SVF products, and improper work practices permit inhalation of the fibers, some workers may experience temporary upper respiratory irritation.
The irritation consists of a nonspecific, temporary respiratory condition, usually manifested by coughing or wheezing. It is mechanically induced by sharp fibers and does not appear to be an allergic reaction. It subsides soon after the worker is removed from exposure and should have no further impact on his or her health and well-being.
Occupational health professionals recommend three levels of precautions for protecting people when they are manufacturing or handling SVF materials.
These precautions effectively reduce airborne SVF exposure and prevent skin and upper respiratory irritation.
Two major mortality studies have been conducted on large groups of workers engaged in the production of either glass or mineral wool, one in Europe and one in the USA.
A third one, more limited, was conducted in Canada on fiberglass production workers.
The researchers found an overall mortality excess among the SVF workers, with the excess particularly evident among workers with less than 1 year of employment.
Among the causes of death that were more numerous were malignant neoplasms, mental disorders, cardiovascular diseases, respiratory diseases, digestive diseases, and external causes.
a. Rock Wool/Slag Wool workers
Simonato et al. reported in 1987 an " excess of lung cancer among rock wool-slag wool workers employed during an early technological phase before the introduction of dust-suppressing agents ", and concluded that " fiber exposure, either alone or in combination with other exposures, may have contributed to the elevated risk ".
In their latest update, they concluded that "the ensemble of these results is not sufficient to conclude that the increased lung cancer risk is related specifically to MMVF( SVF); however, insofar as respirable fibres were a significant component of the ambient pollution of the working environment, they may have contributed to the increased risk "
b. Glass Wool workers
For these workers the report stated that the findings " indicate some excess of lung cancer , clearly reduced once local adjustment factors are applied to national mortality rates, and with no relation to duration of employment nor time since first employment ". No anomalies were found for the continuous glass filament workers.
c. Mesothelioma
Five mesotheliomas have been identified by death certificate, one in the glass wool sub-cohort and four in the rock wool-slag wool sub-cohort. No clear increased risk of mesothelioma has been identified, altough the researchers have concluded that " the possibility of such increase is suggested by the results. "
As with the European study, the U.S. study found a higher overall mortality rate among SVF workers as compared to local and national mortality.
For deaths due to cancer or nonmalignant respiratory disease, the study reported that a positive evidence existed for fine glass and mineral wool production workers.
However, the researchers point out, the data are not consistent with a causal relationship because the excesses in mineral wool and glass microfiber deaths were not directly related to duration of exposure.
The number of deaths from mesothelioma in the study cohort is considered to be within the expected range for the general population.
In the 1985 update, a small but statistically significant excess in respiratory cancer deaths was reported for workers employed in glass wool and mineral wool plants but, the researchers concluded that the evidence of an association appeared " somewhat weaker " than in the 1982 update.
In the 1989 update for the rock wool and slag wool workers, the pattern of findings was generally consistent with findings obseved in previous updates; no consistent evidence remains of an association between lung cancer or non-malignant respiratory diseases and any of the respirable fiber measures considered.
It is a more limited mortality study. The authors reported a statistically significant excess in mortality due to lung cancer among fiberglass production workers. They concluded that the interpretation of this finding was difficult because no relationship existed berween the excess of lung cancer and the lenght of time since first exposure to the fiberglass production environment. It is concluded that the relationship between work and health in the SVF industry should continue to be explored.
In the most widely cited SVF morbidity study, Weil et al.(1983-1984) reported that the study populations were generally healthy, with no respiratory symptoms and no adverse lung functions related to the fiber exposure.
A low incidence of small lung opacities was observed in the chest radiographs (opaque areas sometimes observed in the lungs of workers in potentially dusty trades).
In summarizing their findings they noted that, in general, " the minimal evidence of respiratory effects detected in the investigation , which cannot, at present, be considered clinically significant, is encouraging concerning the question of potential health effects of exposure to MMFV ".
This study was updated and enlarged at the end of the 1980s and the authors concluded that the " results indicate no adverse clinical, functional, or radiographic signs of effects of exposure to MMVFs in these workers ".
Only one known published report is found in the medical literature on health effects of occupational exposure to RCFs. The researchers reported an association between exposures to RCF and the occurrence of pleural plaques, which are usually caused by exposure to asbestos fibers. It was demonstrated that asbestos fibers exposure did not account for the observed association. Also, among the RCF workers, no significant increase was seen in parenchymal changes consistent with interstitial fibrosis.
Implantation studies artificially inject fibers into the body cavities of laboratory animals: Into the pleural (chest) cavity or peritoneal (abdominal) cavity or by instillation into the trachea. Implantation experiments are based on introducing large amounts of fiber into animals by artificial means that bypass normal body defenses. The circumstances of actual exposure are totally different in humans. For these reasons, and because the toxicology induced by implantation of fibers into rodents does not parallel the findings from inhalation studies, implantation studies are not valid for risk assessment or for concluding anything about the human health hazard associated with the inhalation of airborne SVFs.
On the other hand, implantation studies have provided useful information on the mechanisms of fiber toxicity. For example, long fibers (longer than 10 to 20 µm) are most active in implantation as well as in cell culture studies, so scientists have hypothesized that biological activity is directly associated with fiber length.
The animal inhalation model is currently the only valid laboratory method for assessing the hazard to humans of exposure to airborne SVFs.
In recent chronic studies, test SVFs having similar dimensions but different compositions have induced different biological effects. Biological effects approximately parallel fiber biological persistence in the lung. Fiber compositions that are more lung-persistent would accumulate during a chronic exposure and persist longer after termination of exposure and would, therefore, cause more lung irritation than compositions that dissolve or fragment transversely into shorter segments.
Differences in biological effects could also be related to fiber surface reactivity.
In the 1970s and 1980s, seven different rodent inhalational studies reported no tumorigenesis for several forms of fiberglass. In a recent study in rats fiberglass did not induce fibrosis or tumors, whereas crocidolite asbestos induced both types of lung disease. In an other study (preliminary results) in hamsters conducted recently comparing amosite fibers, 901 insulation wool and durable 475 glass demonstrated, as in other studies, that no permanent lung changes were caused by 901 wool. 475 fiberglass induced minimal lung fibrosis and one tumor, a mesothelioma. Amosite asbestos also induced fibrosis, but an earlier and more severe case than that induced by 475 glass, and a low to moderate incidence of mesothelioma. Differences between this study and earlier ones, as far as glass wools are concerned, seem to be related to differences in experimental conditions.
In this study, toxicity somewhat parallels lung biological persistence of fibers. After 12 months of exposure, the number per lung of fibers longer than 20 µm was seven times to eight times higher for high-dose amosite than for 475 glass, which was three to four times higher than for 901 glass.
In agreement with previous findings, these data once again link fiber lenght and biological persistence to toxicity.
Before 1990 three inhalation studies reported no fibrosis or tumors as a result of chronic exposure to mineral wool. One more recent study showed that rats exposed to rock wool developed minimal fibrosis late in the inhalation period.
Two inhalation studies of RCFs were published before 1990, with conflicting results.
The first study (Davis et al.,1984) reported 5% pulmonary fibrosis and 17% pulmonary tumors in rats after 8 months of RCF inhalation.
The second study (Smith et al.,1987) reported RCF-associated fibrosis but no tumors in rats; no fibrosis and only one mesothelioma in hamsters.
In more recent studies rats exposed to RCF developed lung fibrosis, pulmonary tumors (13% in the kaoalin-based RCF group) and pleural mesothelioma. Hamsters exposed to RCF(exposed only to kaolin-based RCF) developed lung fibrosis but no lung cancers but, 42 of 112 animals developed mesotheliomas.
This study presents a striking difference between rat and hamster responses to the same test fiber that opens questions of species-related differences and which species, if either, is representative of humans.
A number of in vitro studies have shown that fiber toxicity to cultured cells is related directly to fiber lenght and perhaps indirectly to fiber diameter. In vitro studies have also contributed much to a better understanding of the molecular mechanisms of fiber-induced injury.
Fibers induce an inflammatory response on the part of the lung and the activated inflammatory cells, in an attempt to destroy foreign invaders, release biologically destructive agents that also injure lung tissue. Repair and cell proliferative responses to injury ensue. If the initiating fibers are biologically persistent, the cascade continues and expands and could result in increasing lung injury, repair mechanisms, and possibly, permanent lung damage such as fibrosis or even tumorigenesis.
Biological persistence of fibers is the ability of fibers to persist in the lung after they have been inhaled.
Biotransformation is any change in dimension, composition, or surface morphology that occurs in a fiber during lung residence. Researchers have only recently begun to scrutinize the mechanisms of fiber biological persistence and biotransformation and their roles in lung injury. In the past, the simple model offered was that fibers that enter the lung and rapidly dissolve are innocuous, those that do not rapidly dissolve are pathogenic.
Now, the situation appears more complex that this according to recent experimental studies on E, 475, 901 glass fibers and rock wool fibers.
In vitro studies have demonstrated widely varying dissolution rates for different fiber compositions. These studies have identified two different types of dissolution:
Fibers can dissolve congruently (i.e., all components dissolve at the same rate) or noncongruently (i.e., certain components dissolve more rapidly than others, leaving a depleted fiber residuum; also called leaching).
Whereas congruent dissolution can lead to the total dissolution and disappearance of fine fibers, noncongruent leaching can weaken the infrastructure of the fiber and thereby trigger transverse fragmentation, resulting in short fiber segments that are biologically less active and more readily removed from the lungs by phagocytic cells.
Leaching-induced changes in fiber chemistry could also have an impact on the biological reactivity of the fiber surface. So, fibers that undergo rapid biotransformation may be less toxic and less likely to cause lung tumours because their altered dimensions or chemistry enhances their clearance and may also decrease their biological reactivity.
Size and shape determine whether a fiber is respirable. These two factors plus specific gravity (density) determine where in the lung the fiber will deposit. Aerodynamic diameter is a term that combines all three of these characteristics.
Fibers longer than 5 µm and less than 1.5 µm in diameter have the greatest potential to reach the target areas of the lung and pleura. Fibers longer than 20 µm may be too long to be removed from the lung by alveolar macrophages.
Altough fiber aerodynamic diameter controls the entry and final site of deposition in the lung, fiber durability is the critical basis for the accumulation of a lung burder of fibers.
Other factors that may affect the intrapulmonary fate of fibers are their rigidity, their surface properties, and the architecture of their ends (smooth, spicule-shaped edges, ect.)
The initial response to deposition of foreign agents, including fibers, into the bronchio-alveolar region is inflammation (alveolitis), which is initiated by lung macrophages (one of the functions performed by this type of cell is phagocytosis or " ingestion " of particulate matter ).
Activated macrophages migrate to the site of fiber deposition and phagocytize (ingest) the fibers. Individual macrophages appear to engulf short fibers completely, but many macrophages may fuse as they engulf longer fibers. The very long fibers may frustrate complete ingestion, resulting in the release of a variety of cell messengers, reactive oxygen species, and proteases from the cell macrophages.
The cell messengers signal the influx and activation of more macrophages and other inflammatory cells.
Biologically destructive agents that are released from lung cells during inflammation attack the lung walls, resulting in tissue necrosis. Tissue injury stimulates tissue repair processes, including cell proliferation and deposition of collagen by fibroblasts within the lung wall. During prolonged tissue repair processes, normal lung morphology is destroyed and replaced by scar tissue that is characterized by an accumulation of collagen in the lung interstitium. This lung scarring is called " lung fibrosis ". Fibrotic scarring can also occur in the mesothelial membranes (pleura) that enclose the lungs and line the thoracic cavity. Fibrotic lesions in the lung and surrounding membranes reduce the efficiency of gas exchange, leaving the individual with an excess of carbon dioxide and a deficit of oxygen.
Very recently, rodent inhalation studies demonstrated for the first time that chronic inhalation of some durable SVF types (RCF, E glass microfibers) at a dose 300-fold greater than typical worker exposure could also be associated with fibrosis and thoracic cancers.
475 durable glass as microfibers may also induce mesothelioma in hamsters at the same level of exposure.
Lung cancer could develop as a by-product of the chronic fibrosis that results from the chronic lung irritation and caused by durable lung fibers. This mechanism would require that the fiber be very biologically persistent in the lung. Tobacco smoke is suggested to be a crucial factor in the development of fiber-related cancers. A second possible mechanism is that inorganic fibers may act by direct genotoxic action to induce neoplams.
Malignant mesothelioma is cancer of the mesothelial membranes, which cover the internal organs and line the inner surfaces of the abdominal and thoracic cavities.
After chronic inhalation of high concentrations of RCF, 42% of hamsters but only 1-3% of rats developed thoracic mesotheliomas. As with lung cancer, the mechanisms of fiber induction of mesothelioma are not well understood.
After inhalation and deposition of fibers, the next step in the development of fiber-associated mesothelioma may be the translocation of fibers through the lung wall into the pleural membranes.
Subsequent steps may involve the development and advancement of pleural fibrosis in the same way that lung fibrosis is theorized to be a mechanism in the development of lung cancer.
As with lung cancer mechanisms, a second potential mechanism of mesothelioma development would be direct genotoxicity of the fibers in the pleural space.
Altough not completely understood, the mechanisms of fiber-induced biological effects are believed to include the following:
In addition, fibers may also induce neoplastic changes directly in the genetic material of the cell.
Also affecting the potential pathogenesis are other factors that compromise pulmonary health, including previous or current disease or exposure to toxic cofactors such as cigarette smoke, other dusts, or industrial fumes.
It is important to note that lung defense mechanisms can be overwhelmed by extreme experimental exposure concentrations, resulting in lung injury that is not specific to the particle type. So, at overload concentrations, lung injuries can be induced by innocuous dusts that, at normal exposure levels, would be cleared from the lung before they are able to accumulate sufficiently to inflict injury.
Many recent rodent studies were conducted at exposure levels 300 times greater than fiber aerosols typically experienced by SVF workers (Research and Consulting Co.Switzerland).
Each year, industrial hygienists analyze more than 1,000 occupational exposure samples in at least 20 SVF manufacturing plants in North America and Europe. Air samples are also taken during insulation installation and in buildings where SVF insulation and air filtration products are in use.
NIOSH method 7400 and the WHO reference method established procedures for microscopically determining the number of respirable fibers per cubic centimeter of air.
In general, exposure to SVFs during manufacture, installation and final use has been very low or undetectable.
In SVF manufacturing workplaces, airborne fiber exposures have typically been less than 0.2 fiber per cubic centimeter, with total particulate matter less than 1.0 mg/m3.
During installation of fiberglass, fiber exposures averaged less than 0.5 fiber per cubic centimeter, with a range of 0 to 20 fibers per cubic centimeter, and total particulate matter averaged less than 4.2 mg/m3, with a range of 0.04 to 114.00 mg/m3.
Air samples were analyzed from a number of public buildings in which fiberglass air filters were in use or in which fiberglass insulation had been installed; these analyses demonstrated no significant fiberglass exposure to the building occupants.
Airborne concentrations of dust and fibers in U.S. mineral wool plants are generally higher than in U.S.glass wool facilities. Exposures during application or installation are also typical higher for mineral wool products than for similar glass wool products. Industrial hygiene monitoring data obtained on a regular basis at locations where RCF products are manufactured show that exposures are generally less than 1.0 fiber per cubic centimeter and often lower than 0.2 fiber per cubic centimeter. During installation of RCF products, exposures can be 1 to 5 fibers per cubic centimeter or higher if appropriate engineering controls and work practices are not followed.
A fiber may be defined as a lenghty particle whose lenght/diameter ratio is equal or larger than 3. In order to reach the lung alveolar region in man, a fiber must have an aerodynamic diameter of less than 10 µm.
When conducting occupational exposure studies to man-made fibers, only fibers considered hazardous to workers due to their granulometric properties, are considered:
QUEBEC'S EXPOSURE LIMITS |
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Substance | VEMP | Notes |
1. Insulating wool fiber, slag wool | 1 fiber/cm³ | C3, EM |
2. Insulating wool fiber, rock wool | 1 fiber/cm³ | C3, EM |
3. Insulating wool fiber, glass wool | 2 fibers/cm³ | C3 |
4. Refractory fibers, (ceramic or others) | 1 fiber/cm³ | C3 |
5. Glass microfibers | 1 fiber/cm³ | - |
C2: suspected carcinogen to humans
C3: confirmed carcinogen to animalsbr />
EM: substance that should be kept at the lowest practicable level
To accurately assess the toxicologic potential of a substance in the workplace, all other substances present in the environment must be considered.
Many chemicals may be present in man-made fibers, which is not the case for asbestos fibers.
During the fabrication process many chemicals may be added and account for up to 25 % of the weight of these fibers, which may also be termed inorganic non-metallic artificial fibers.
The chemicals added may be:The presence of these additives may make research on the toxicology of these fibers more complicated.
The potential cumulative effects of exposure to all these materials must be considered in any operation to develop a sound plan for employee and environmental health and safety.
In 1971, the International Agency for Reserach on Cancer (IARC) iniated a program by which to evaluate data regarding the carcinogenic risk of chemicals to humans.
In 1987, the IARC appointed a working group of 20 scientists to evaluate the carcinogenic risk of exposure to SVFs.
IARC ClassificationGlass wool was designated in group 2B.
Continuous filament (glass textile) was designated as group 3.
Rock wool was clasified as group 2B.
Slag wool was classified as group 2B.
RCF(refractory ceramic fiber) was designated as a group 2B substance.
The IPCS is a joint venture of the United Nations Environment Program, the International Labor Organization and the WHO.
The1988 report, " Man-made Mineral Fibres ", concluded the following:
They also recommended protective equipment to guard against a potential elevation in lung cancer risk for workers engaged in activities in which elevated airborne exposure levels are possible.
For SVF in general the IPCS stated, " The overall picture indicates that the possible risk of lung cancer among the general public is very low, if there is any at all, and should not be a cause for concern if the current low levels of exposure continue ".
Whenever there exists a potential for employees to be exposed to substsnces that either are known to be harmful or have not been completely evaluated, the first step is to mini-mize exposure to the lowest practicable level.
In SVF occupational settings, modifications to the product design can sometimes reduce the amount of dust that it releases during manufacture or installation.
Exhaust ventilation can remove dusts at their points of origin. Appropriate work practices can also limit the amount of dust generated; for exemple, vacuum cleaning is better than dry-sweeping with a broom or with compressed air.
SVF workers can further protect themselves by wearing safety glasses or goggles to prevent eye exposure, long-sleeved shirts and long pants to minimize skin exposure, and respiratory protection to minimize dust inhalation.
A careful evaluation of the workplace should be conducted to determine the appropriate devices to be used in an individual situation.
Whenever employees are exposed to potentially harmful substances, a program should be established to monitor their exposure levels and health routinely.
First, exposure ranges and averages should be determined for each operation or task.
Next, the appropriate type of personal protective equipment should be determined for each task.
A medical surveillance program should be established, including a review of general health, occupational history, physical examination, clinical chemistries and blood count, pulmonary function testing, a baseline chest radiograph, and other testing as indicated by the occupational history.
For SVF workers, the focus should be on respiratory and dermatologic health.
Exposure and health monitoring should continue on a regular basis (e.g., yearly) or whenever processes or products change. Findings should be reviewed regularly, both for individuals and groups.
The ban on the use of asbestos resulted in a larger and larger use of substitution materials in many industrial processes and in particular the use of man-made vitreous fibers (MMVF).
In rodents, inhalational studies show that glass insulation wools and slag wool produced no permanent injury, even after 2 years of exposure to high concentrations (at least 300-fold the concentrations to which human SVF workers typically are exposed). In recent rodent inhalational studies, two durable SVFcompositions were associated with permanent lung injury: rock wool (MMVF21) induced fibrosis late in the study, and RCF induced fibrosis and tumorigenesis. Other durable fibers are pathogenic to animals: glass microfiber E may also induce fibrosis and tumorigenesis in rats, fiber glass 475 induces fibrosis and mesothelioma in hamsters but not in rats.
In man, the main part of known health effects comes from data collected among workers of industries producing these fibers, where the levels of exposure were low, much lower than those encountered in many professional situations by the finished product users.
Even if the relationship to the exposure to rockwool fibers/slag wool fibers is not clearly established, the observation of an excess of bronchopulmonary cancers among workmen producing these fibres must prompt us to be vigilant and to control levels of exposure to these fibers in the work environment. The SMRs for bronchopulmonary cancer are lower among workmen of glass wool production than among workmen of rockwool/slag wool production.
Taking into account data observed in experiments (excess of tumours) and preliminary information obtained from man (suspicion of an excess of benign pleural pathologies, and of respiratory functional impairment of the obstructive type), an attitude even more careful is essential with respect to refractory ceramic fibres.
These fibres were classified in category 2 (similar substances to cancerogenic substances for man) by the European Communities. Nothing currently makes it possible to affirm that a risk of nonmalignant respiratory pathology exists for man with rock, glass, and slag fibers. Nevertheless, experimental data showed a real pathogenic effect for levels of exposure close to those producing the same effects with asbestos. Certain fibers, as some made from glass, appear sufficiently soluble to have no irreversible effects. Others like ceramic fibers are more suspicious.
The absence of sufficient experience must prompt us to pursue epidemiologic and experimental studies, and to introduce an effective prevention policy.
By Edouard Bastarache
Typecodes |
Article by Edouard Bastarache
Edouard Bastarache is a well known doctor that has written many articles on the subject of toxicity of ceramic materials and books on technical aspects of ceramics. He writes in both English and French. |
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Hazards |
Asbestos: A Difficult-to-Repace Material
|
Hazards |
Propane Toxicology
Hazards of using this material in the ceramic industry and process |
Hazards |
Man-Made Vitreous Fibers Safety Update
A 2021 MMVF safety update, with many references, from NAIMA (North American Insulation Manufacturers Association) |
Materials |
Ceramic Fiber
|
URLs |
http://www.rcfc.net/
Refractory Ceramic Fibers Coalition Website |
URLs |
https://thermcraftinc.com/manufacturing-ceramic-fiber-insulation/
Information on how ceramic fibre (RCF) is made |
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