Chronic Inhalation Toxicity and Carcinogenicity Testing of Respirable Fibrous Particles

Vu, Vanessa; Barrett, J. Carl; Roycroft, Joseph H.; Schuman, Loretta D.; Dankovic, David A.; BBaro, Paul; Martonen, T. B.; Pepelko, William E.; Lai, David Y.

doi:10.1006/rtph.1996.0128

Cited by 32 publications

(13 citation statements)

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“…Failure to rigorously describe NMs may conceal potential hazardous properties. 9 Experiments performed on laboratory animals have revealed that certain classes of nanomaterials, upon entering the alveoli of the lung, are small enough to then pass directly to the bloodstream and induce inflammatory responses in other organs (Vu et al 1996;Kayat et al 2011). Owing to quantum effects that dominate at the nanoscale, the behaviour of nanoparticles is in general difficult to predict and is not intuitively accessible (Roduner 2006).…”

Section: Emerging Regulatory Responsementioning

confidence: 99%

Engineered nanomaterials: risk perception, regulation and insurance

McAlea

Mullins

Murphy

et al. 2014

Journal of Risk Research

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Concerns surrounding the health risk of engineered nanomaterials, effective regulation and the lack of specifically tailored insurance products for the nanotechnology sector are putting the industry's long-term economic viability at risk. From the perspective of the underwriter, this article speculates on the relationship between risk perception, regulation and insurability. In the nanotechnology sector, regulators are currently failing to keep pace with innovation, and insurers generally lack guiding principles for underwriting occupational risk from nanomaterial exposure. Such vulnerabilities when combined with misguided risk perceptions can lead to the overpricing of risk transfer and ill-conceived regulatory initiatives, thus potentially exhausting resources and stifling innovation in the sector. In the absence of well-developed regulatory protocols, the insurance industry has, and will continue, to occupy a key role as an effective lobby in terms of improved risk management practice. We suggest that the insurance industry will increasingly rely on control banding frameworks and 'risk mitigation at source' methods developed in conjunction with their clients to manage severe acute diversifiable risks. Long tail risk will continue to represent a serious challenge to insurers and regulators. In the meantime, insurers will have to bridge their current needs with improvised solutions. As an example of one possible solution, we outline a framework that utilizes financial instruments to hedge an insurer's exposure to uncertain estimates of these long-term risks.

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Section: Emerging Regulatory Responsementioning

confidence: 99%

Engineered nanomaterials: risk perception, regulation and insurance

McAlea

Mullins

Murphy

et al. 2014

Journal of Risk Research

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“…In a 1995 meeting sponsored by the U.S. EPA and in collaboration with NIEHS, NIOSH, and OSHA, a panel of expert fiber toxicologists discussed toxicity testing of fibers (Vu et al, 1996). The panel agreed that animal chronic inhalation studies were the appropriate, current method for assessing the potential human health effects of inhalation exposure to fibrous dusts.…”

Section: Criteria For Establishing the Mtd In Fiber Inhalation Studiesmentioning

confidence: 99%

Studies on the Inhalation Toxicology of Two Fiberglasses and Amosite Asbestos in the Syrian Golden Hamster. Part I. Results of a Subchronic Study and Dose Selection for a Chronic Study

Hesterberg¹,

Axten²,

McConnell

et al. 1999

Inhalation Toxicology

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A multidose, subchronic inhalation study was used to estimate the maximum tolerated dose (MTD) of 901 fiberglass (MMVF10.1) for a chronic inhalation study using hamsters. Subchronic study results indicated that 30 mg/m(3) [250-300 WHO fibers (>5 microm long)/cm(3) and 100-130 fibers/cm(3) >20 microm long] meets or exceeds the estimated MTD, and chronic study results confirmed this. For the subchronic study, hamsters were exposed 6 h/day, 5 days/wk, for 13 wk to MMVF10.1 at 3, 16, 30, 45, and 60 mg/m(3) (36, 206, 316, 552, or 714 WHO fibers/cm(3)), then monitored for 10 wk. Results demonstrating MTD were: inflammatory response (all fiber exposures); elevated lung cell proliferation with @ges;16 mg/m(3); lung lavage neutrophil elevations with @ges;16 mg/m(3) and lactate dehydrogenase (LDH) and protein elevations with > or = 30 mg/m(3); and persistent abnormal macrophage/fiber clumps in lungs exposed to 45 and 60 mg/m(3), which suggest overloading of clearance mechanisms. For the chronic study, hamsters were exposed for 78 wk to MMVF10a (901 fiber glass) or MMVF33 (special-application 475 fiberglass) at approximately 300 WHO fibers/cm(3) ( approximately 100 fibers/cm(3) @gt;20 @mu;m long), or to amosite asbestos at an equivalent concentration and 2 lower concentrations. All fiber-exposed animals had pulmonary inflammation, elevated lung lavage cells, and increased lung cell proliferation. Between 52 and 78 wk of exposure, lung burdens of all fibers increased at an accelerated rate, suggesting impairment of clearance mechanisms. MMVF33 and amosite induced fibrosis and pleural mesothelioma. These findings substantiate that exposures in the chronic study adequately tested the toxic potential of fiberglass.

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“…Two expert advisory panels recommended the rat as the best available animal model for predicting the hazard and risk of inhaled particles and fibers in humans (Vu et al, 1994;ILSI, 2000). These evaluations also point out that the rat is more responsive to inhaled particles than is the mouse or hamster.…”

Section: To the Editormentioning

confidence: 99%