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Human Exposure and Risk Assessment for Naturally Occurring Asbestos

May 21st, 2010 Comments off

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Asbestos is a general name given to a group of naturally occurring silicate minerals with a tendency to separate into fibers or fiber bundles. The fibers have high tensile strength, low heat transfer, chemical resistance, and heat resistance. These properties make asbestos useful for a number of industrial applications, including thermal insulations and fireproofing, friction materials such as automotive brake pads, and fiber reinforcement in cementitious materials…

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Although asbestos is a versatile material with many commercial applications, it also a known human carcinogen. Epidemiological data consistently indicate an increased incidence of cancer in occupationally exposed individuals. Asbestos exposure occurs primarily through inhalation of fibers in asbestos dust. Animal inhalation studies show consistently similar findings for lung cancer and mesothelioma. Animal and epidemiological ingestion study data are insufficient to judge carcinogenicity due to ingestion. Asbestos regulation has been based on a linear dose-response relationship between exposure and adverse health effects (risk increases as total dose increases) and on the lack of a known exposure threshold below which no asbestos-related health effects have been observed. Much of the available epidemiological data cover occupational exposures, which are frequently higher than environmental exposures.

Since asbestos is a naturally-occurring mineral, however, there are areas of the United States in which geological deposits of asbestos minerals pose a potential environmental exposure risk. Asbestos also occurs as a contaminant in some commercially mined minerals, such as vermiculite. The most well-known case of exposure to naturally-occurring asbestos may be the case of Libby, Montana. Asbestos-contaminated vermiculite was mined in Libby from 1919 until the mine was closed in 1990. In response to local concerns and media coverage of the local population’s exposure to the asbestos-contaminated vermiculite, EPA sent an emergency response team to Libby in 1999 to collect air, soil, dust, and insulation samples from businesses and homes. Libby was added to EPA’s Superfund National Priorities List in 2002. Asbestos-related lung diseases have been observed in the Libby population. Exposure scenarios in this case include occupational exposures in the mining process, exposure of family members through “take-home” dust, environmental exposures due to ambient airborne asbestos concentrations, and exposure of residents due to vermiculite-containing insulations and soil conditioners used in and around their homes.

Although the Libby, Montana, situation may be the best known case of exposure to naturally occurring asbestos in the United States, there are other areas of the country in which asbestos deposits result in potential exposure. The presence of naturally occurring asbestos in exposed soils in El Dorado Hills, California, has been well documented by State and Federal agencies. In response to a citizen’s petition to evaluate asbestos-related health risks in the community, EPA contracted to conduct a multimedia assessment of the area in 2003 to evaluate the potential for inhalation exposure to naturally occurring asbestos in disturbed soils. That assessment concluded through activity-based sampling that airborne asbestos concentrations were elevated in the breathing zone for both children and adults when soils were disturbed (Ladd, 2005).

Unlike occupational asbestos exposures, which may be controlled with personal protective equipment and specialized work practices, exposure to naturally occurring asbestos in native soils is not easily controlled. Exposed individuals may not even realize they have been exposed during outdoor activities. While occupational exposures generally affect adults of working age, exposure to naturally occurring asbestos minerals may also affect children and the elderly. Adverse health effects resulting from exposure to asbestos have been anecdotally documented as far back as ancient Rome, where slaves weaving asbestos fibers into textile products became weakened due to breathing problems and suffered premature death. More recent awareness of escalating asbestos-related respiratory disorders in the 1960s and early 1970s led EPA to add asbestos in 1971 to the list of materials regulated by the National Emissions Standard for Hazardous Air Pollutants (NESHAP), and to promulgate regulation under the Asbestos Hazard Emergency Response Act (AHERA) in 1986 to address asbestos in schools. AHERA covers asbestos-containing materials inside school buildings and, therefore, works to protect a susceptible subpopulation (children).

While there is strong evidence of a causal link between inhalation of asbestos particles and the development of debilitating respiratory disease and cancers, the specific mechanisms by which asbestos minerals cause disease are still not fully understood. The roles that morphology, fiber length, chemistry, and solubility in biological fluids (biopersistence) play in asbestos toxicity are still an area of vigorous debate. As noted by Fubini and Fenoglio (2007), particle toxicology is a distinct study area. Particle toxicants, in which surface chemistry and surface topography play a significant role in interaction with living tissues, behave differently than molecular toxicants. A particle’s surface structure and surface chemistry are affected by factors such as the mechanical processes that generate the particle, weathering processes, and adsorption of chemical contaminants onto the particle surface. For this reason, two particles with the same general chemical composition may have different surface chemistry.

In the case of mineral particles, properties relevant to toxicity include fibrous morphology, surface features such as sharp edges or fracture faces, surface reactivity related to covalent and ionic bonds, the presence of surface contaminants, and biopersistence. Asbestos particles have some toxicity characteristics that are different from other mineral dusts. Although fibrous morphology plays a part in toxicity, not all mineral fibers are equally toxic. There is some evidence that carcinogenic potency varies with asbestos mineral type and the geographic area from which the asbestos originates (EPA IRIS). It is generally agreed that chrysotile asbestos is less toxic than the other regulated asbestos minerals in relationship to mesothelioma, a cancer of the lining of the lungs and abdominal cavity.

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Human Exposure and Risk Assessment for Naturally Occurring Asbestos (Part 2)

May 21st, 2010 Comments off

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There is not clear evidence of lower chrysotile toxicity in relationship to lung cancer and asbestosis, a debilitating scarring of the lung tissues. Evidence, such as that reviewed by Hardy in 1995, suggests that iron also plays a part in asbestos toxicity. Iron is present in all asbestos minerals. Iron ions on the surface of asbestos fibers may be catalytic sites for free radical and reactive oxygen species (ROS) generation, resulting in the initiation or promotion of cancer.

EPA’s carcinogenicity assessment dates back to 1986. The lung cancer model in that assessment (Nicholson, 1986) assumes a linear function of cumulative asbestos exposure in units of fibers-years/ml as measured with phase contrast microscopy, and can be expressed as follows: IL IE(1+KL*f*d), where: IL lung cancer incidence observed or projected in an exposed population IE lung cancer expected in the absence of exposure KL= proportionality constant measure of the carcinogenic potency of exposure f intensity of exposure (fibers/ml) d duration of exposure (years) The model assumes equal potency for all six regulated asbestos types and all asbestos fibers greater than 5 μm in length. The 1986 assessment document does point out that fiber size distribution varies with asbestos type and mineral processing, and accepts that length and width are important variables in fiber carcinogenicity in animal studies. Stanton et al (1981) developed the “Stanton Hypothesis,” which suggested that long thin fibers were the most toxic. Later studies, such as those reviewed by Dodson et al, suggested that all fiber sizes may contribute, to some extent, to asbestos toxicity. One source of uncertainty in asbestos exposure estimates is the uncertainty of conversions between analytical measurements performed with PCM and measurements performed with transmission electron microscopy (TEM).

Asbestos unit risk is based on fiber counts made with PCM because PCM is typically the method used for measurements in the occupational environment. Unfortunately, PCM is not fiber specific. All fibers are counted, regardless of identity. PCM also does not have the resolution necessary to image smaller fibers, generally resolving fibers longer than 5 μm and greater than 0. 4 μm in diameter. Transmission electron microscopy (TEM) resolves much shorter and thinner fibers and allows for identification of fibers based on chemical composition and selected area electron diffraction (SAED) of the mineral’s crystal structure. The correlation between PCM and TEM is highly uncertain. Asbestos measurement techniques and the level of understanding of asbestos toxicity have improved substantially since EPA’s 1986 assessment document.

A proposed updated methodology for conducting asbestos risk assessments (Berman and Krump, 2003) is under review at this time. The proposed methodology, which distinguishes between asbestos types and fiber sizes in assessing risk, is a topic of debate. The report on EPA’s peer consultation workshop to discuss the proposed methodology (Eastern Research Group, 2003) documents several discussion topics. Issues under discussion include fiber diameter and length (what size cut-off points to use in considering fibers), the use of different carcinogenic potency factors for different asbestos fiber types for lung cancer versus mesothelioma, how to address mineral cleavage fragments of equal dimension and biopersistence as fibers, the potency of unregulated asbestos minerals, statistical analysis methods, consideration of the synergistic impact of cigarette smoking, and localized exposures to naturally occurring asbestos such as that in California. The potential for health risks associated with exposure to asbestos minerals continues to be a public concern. Much of the epidemiological asbestos data studied over the past several decades has focused on occupational exposure. Since asbestos is a generic term used to identify a group of naturally-occurring minerals, however, there are areas of the United States in which geological deposits of asbestos minerals pose a potential environmental exposure risk. Unlike occupational asbestos exposures, which can be controlled with personal protective equipment and specialized work practices, exposure to naturally occurring asbestos may not be easily controlled and may impact susceptible subpopulations. Given the asbestos toxicity questions that remain and the vigorous research debate, it is obvious that asbestos is still a relevant exposure and risk assessment topic.

References

Berman, D. W. and Krump, K. (2003). “Technical Support Document for a Protocol to Assess Asbestos-Related Risk – Final Draft. ” Report No. EPA 935. 4-06600/8-84/003F, Prepared for U. S. EPA Office of Solid Waste and Emergency Response, Washington, DC.

Bernarde, M. (1990). Asbestos The Hazardous Fiber. CRC Press: Florida.

Dodson, R. Atkinson, M. and Levinson, J. (2003). “Asbestos Fiber Length as Related to Potential Pathogenicity: A Critical Review,” American Journal of Industrial Medicine, 44: 291-297.

Eastern Research Group, Inc. (2003). “Report on the Peer Consultation Workshop to Discuss a Proposed Protocol to Assess Asbestos-Related Risk. ” Contract No. 68-C-98-148, Prepared by Eastern Research Group, Inc. for U. S. EPA Office of Solid Waste and Emergency Response, Washington, DC.

Fubini, B. and Fenoglio, I. (2007). “Toxic Potential of Mineral Dusts,” Elements, 3: 407-414. Hardy, J. and

Aust, A. (1995). “Iron in Asbestos Chemistry and Carcinogenicity,” Chemical Reviews, 95(1): 97-118.

Ladd, K. (2005). “El Dorado Hills Naturally Occurring Asbestos Multimedia Exposure Assessment, Preliminary Assessment and Site Inspection Report Interim Final. ” Contract No. 68-W-01-012, Prepared by Ecology and Environment, Inc. Superfund Technical Assessment and Response Team (START) for U. S. EPA Region IX. Nicholson, W. J. (1986). “Airborne Asbestos Health Assessment Update. ” Report No. EPA/600/8-84/003F, Prepared for U. S. EPA Environmental Criteria and Assessment Office, Research Triangle Park, NC.

Stanton M. F. Layard M. Tegeris E. Miller E. May M. Morgan E. and Smith A. (1981). “Relation of Particle Dimension to Carcinogenicity in Amphibole Asbestoses and Other Fibrous Minerals. ” Journal of the National Cancer Institute, 67: 965-975.

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Human Exposure and Risk Assessment for Naturally Occurring Asbestos (Part 3)

May 21st, 2010 Comments off

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Summary/Toxicological Review for Asbestos (CASRN 1332-21-4) viewed at Integrated Risk Information System (IRIS) website, USEPA, http://www. epa. gov/ncea/iris/subst/0371. htm, viewed February 1, 2008.

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Cash 4 Clunkers: Scam 4 Taxpayers

August 6th, 2009 No comments

If you’ve been following the news at all, you have probably heard your fair share of Obama PropagandaRama. One such item on the ObamAgenda is the Cash for Clunkers scheme, where the government puts up the funds for a $4500 credit toward the purchase of a new car if someone brings in a “clunker” to the dealership. The objective, so the Obamanauts say, is to put more fuel efficient cars on the road AND save the auto industry in America.

Bollocks. What a massive load of bollocks. If you think that paying someone to destroy wealth is beneficial to anyone except the payee (and anyone else sitting on the gravy train along the way), you need to seriously reevaluate whether you should be forming opinions on economic issues at all.

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