Carbon black should not be classified as a human carcinogen based on rodent bioassay data

Rausch, L.J; Bisinger, E.C; Sharma, Archana

doi:10.1016/j.yrtph.2004.04.004

Cited by 19 publications

(7 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…To clarify the effects of nano-scaled Ni, C-NiNPs were served as the control nanoparticles for NiNP due to carbon-based substance is critical for reducing the inherent reactivity of nanoparticles with biomolecules. Also, carbon materials are considered to be less-bioreactive substances in biological systems [19]. Based on the results of FE-SEM and EDX, we found that the size of NiNPs varied and that they had a higher Ni content than C-NiNPs.…”

Section: Discussionmentioning

confidence: 88%

Dysfunction of methionine sulfoxide reductases to repair damaged proteins by nickel nanoparticles

Feng¹,

Huang

Chuang

et al. 2015

Chemico-Biological Interactions

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 88%

Dysfunction of methionine sulfoxide reductases to repair damaged proteins by nickel nanoparticles

Feng¹,

Huang

Chuang

et al. 2015

Chemico-Biological Interactions

View full text Add to dashboard Cite

“…Rapid alveolar uptake of rodent carcinogens, such as benzo[a]pyrene adsorbed onto diesel particulates, has been reported and has been proposed to enhance the tumorigenic effect, because DEEinduced lung tumors are probably of alveolar origin (Gerde et al, 2001;Iwai et al, 1997). However, a major contribution of the volatile or absorbed constituents of DEE can be excluded because intratracheal instillation of DEE particulates alone or exposure to carbon black provoked both inflammatory changes and lung tumors, whereas with particle-filtered DEE vapor alone, a marked reduction of the inflammatory and tumorigenic response was observed (Brightwell et al, 1989;Ishihara & Kagawa, 2003;Kato et al, 2000;Rausch et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

Chronic Nose-only Inhalation Study in Rats, comparing Room-aged Sidestream Cigarette Smoke and Diesel Engine Exhaust

Stinn

Teredesai

Anskeit

et al. 2005

Inhalation Toxicology

View full text Add to dashboard Cite

Nose-only exposure of male and female Wistar rats to a surrogate for environmental tobacco smoke, termed room-aged sidestream smoke (RASS), to diesel engine exhaust (DEE), or to filtered, fresh air (sham) was performed 6 hours/day, 7 days/week for 2 years, followed by a 6-month post-exposure period. The particulate concentrations were 3 and 10 mg/m3. Markers of inflammation in bronchoalveolar lavage showed that DEE (but not RASS) produced a dose-related and persistent inflammatory response. Lung weights were increased markedly in the DEE (but not RASS) groups and did not decrease during the 6-month post-exposure period. Bulky lung DNA adducts increased in the RASS groups, but not in the DEE groups. Cell proliferation in the lungs was unaffected by either experimental treatment. Histopathological responses in the RASS groups were minimal and almost completely reversible; lung tumors were similar in number to those seen in the sham-exposed groups. Rats exposed to DEE showed a panoply of dose-related histopathological responses: largely irreversible and in some cases progressive. Malignant and multiple tumors were seen only in the DEE groups; after 30 months, the tumor incidence (predominantly bronchiolo-alveolar adenomas) was 2% in the sham-exposed groups, 5%in the high RASS groups, and 46% in the high DEE groups (sexes combined). Our results suggest that in rats exposed to DEE, but not to RASS, the following series of events occurs: particle deposition in lungs --> lung "overload" --> pulmonary inflammation --> tumorigenesis, without a significant modifying role of cell proliferation or DNA adduct formation.

show abstract

“…Longer-term studies in rats exposed to high airborne TiO 2 concentrations indicate impairment of lung clearance mechanisms, fibrosis, and cancer (Heinrich et al, 1995;Bermudez et al, 2004) by a mechanism that is not considered relevant for humans (i.e. lung overload and greater reactivity in the rat lung; see Fryzek et al, 2003;Borm et al, 2004;Rausch et al, 2004;Hext et al, 2005;Warheit and Frame 2006;Baan et al, 2006). Warheit et al (2007a) described toxicity information for TiO 2 , comprising a minimum base set of tests in accordance with the ED/DuPont framework for responsible development of products containing nanomaterials (Medley et al, 2007).…”

Section: Inorganic Particulatesmentioning

confidence: 99%

Application of Toxicology Studies in Assessing the Health Risks of Nanomaterials in Consumer Products

Tsuji¹,

Mowat²,

Donthu³

et al. 2009

Nanotoxicity

View full text Add to dashboard Cite

Carbon black should not be classified as a human carcinogen based on rodent bioassay data

Cited by 19 publications

References 33 publications

Dysfunction of methionine sulfoxide reductases to repair damaged proteins by nickel nanoparticles

Dysfunction of methionine sulfoxide reductases to repair damaged proteins by nickel nanoparticles

Chronic Nose-only Inhalation Study in Rats, comparing Room-aged Sidestream Cigarette Smoke and Diesel Engine Exhaust

Application of Toxicology Studies in Assessing the Health Risks of Nanomaterials in Consumer Products

Contact Info

Product

Resources

About