Response to letters regarding “Cosmetic talc as a risk factor for pleural mesothelioma: a weight of evidence evaluation of the epidemiology”

Finley, Brent L.; Benson, Stacey; Marsh, Gary M.

doi:10.1080/08958378.2018.1438540

Cited by 4 publications

(4 citation statements)

References 19 publications

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“…2017 ). Consistent with prior studies that reported metal nanoparticles in the brain of animals ( Klocke et al. 2018 ) and humans ( González-Maciel et al.…”

Section: Discussionsupporting

confidence: 91%

The Effects of Chronic Exposure to Ambient Traffic-Related Air Pollution on Alzheimer’s Disease Phenotypes in Wildtype and Genetically Predisposed Male and Female Rats

Patten

Valenzuela

Wallis

et al. 2021

Environ Health Perspect

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Background: Epidemiological data link traffic-related air pollution (TRAP) to increased risk of Alzheimer’s disease (AD). Preclinical data corroborating this association are largely from studies of male animals exposed acutely or subchronically to high levels of isolated fractions of TRAP. What remains unclear is whether chronic exposure to ambient TRAP modifies AD risk and the influence of sex on this interaction. Objectives: This study sought to assess effects of chronic exposure to ambient TRAP on the time to onset and severity of AD phenotypes in a preclinical model and to determine whether sex or genetic susceptibility influences outcomes. Methods: Male and female TgF344-AD rats that express human AD risk genes and wildtype littermates were housed in a vivarium adjacent to a heavily trafficked tunnel in Northern California and exposed for up to 14 months to filtered air (FA) or TRAP drawn from the tunnel and delivered to animals unchanged in real time. Refractive particles in the brain and AD phenotypes were quantified in 3-, 6-, 10-, and 15-month-old animals using hyperspectral imaging, behavioral testing, and neuropathologic measures. Results: Particulate matter (PM) concentrations in TRAP exposure chambers fluctuated with traffic flow but remained below 24-h PM with aerodynamic diameter less than or equal to 2.5 micrometers ( ) U.S. National Ambient Air Quality Standards limits. Ultrafine PM was a predominant component of TRAP. Nano-sized refractive particles were detected in the hippocampus of TRAP animals. TRAP-exposed animals had more amyloid plaque deposition, higher hyperphosphorylated tau levels, more neuronal cell loss, and greater cognitive deficits in an age-, genotype-, and sex-dependent manner. TRAP-exposed animals also had more microglial cell activation, but not astrogliosis. Discussion: These data demonstrate that chronic exposure to ambient TRAP promoted AD phenotypes in wildtype and genetically susceptible rats. TRAP effects varied according to age, sex, and genotype, suggesting that AD progression depends on complex interactions between environment and genetics. These findings suggest current regulations are insufficient to protect the aging brain. https://doi.org/10.1289/EHP8905

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“…2017 ). Consistent with prior studies that reported metal nanoparticles in the brain of animals ( Klocke et al. 2018 ) and humans ( González-Maciel et al.…”

Section: Discussionsupporting

confidence: 91%

The Effects of Chronic Exposure to Ambient Traffic-Related Air Pollution on Alzheimer’s Disease Phenotypes in Wildtype and Genetically Predisposed Male and Female Rats

Patten

Valenzuela

Wallis

et al. 2021

Environ Health Perspect

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“…Then, multiple epidemiological studies have validated that there is a concentration-response relationship between airborne PM 2.5 and its harmful effects on respiratory system [5,[7], [8], [9]]. In mice models, a recent study found that the severity of lung injury caused by ambient PM exposure is associated with cumulative dose [10]. Acute exposure to low doses of fine PM by intranasal instillation also induced lung inflammation and oxidative stress in a dose-dependent manner [11].…”

Section: Introductionmentioning

confidence: 99%

The effect of exposure time and concentration of airborne PM2.5 on lung injury in mice: A transcriptome analysis

et al. 2019

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The association between airborne fine particulate matter (PM 2.5 ) concentration and the risk of respiratory diseases has been well documented by epidemiological studies. However, the mechanism underlying the harmful effect of PM 2.5 has not been fully understood. In this study, we exposed the C57BL/6J mice to airborne PM 2.5 for 3 months (mean daily concentration ~50 or ~110 μg/m 3 , defined as PM 2.5 –3L or PM 2.5 –3H) or 6 months (mean daily concentration ~50 μg/m 3 , defined as PM 2.5 –6L) through a whole-body exposure system. Histological and biochemical analysis revealed that PM 2.5 –3H exposure caused more severe lung injury than did PM 2.5 –3L, and the difference was greater than that of PM 2.5 –6L vs PM 2.5 –3L exposure. With RNA-sequencing technique, we found that the lungs exposed with different concentration of PM 2.5 have distinct transcriptional profiles. PM 2.5 –3H exposure caused more differentially expressed genes (DEGs) in lungs than did PM 2.5 –3L or PM 2.5 –6L. The DEGs induced by PM 2.5 –3L or PM 2.5 –6L exposure were mainly enriched in immune pathways, including Hematopoietic cell lineage and Cytokine-cytokine receptor interaction, while the DEGs induced by PM 2.5 –3H exposure were mainly enriched in cardiovascular disease pathways, including Hypertrophic cardiomyopathy and Dilated cardiomyopathy. In addition, we found that upregulation of Cd5l and reduction of Hspa1 and peroxiredoxin-4 was associated with PM 2.5 -induced pulmonary inflammation and oxidative stress. These results may provide new insight into the cytotoxicity mechanism of PM 2.5 and help to development of new strategies to attenuate air pollution associated respiratory disease.

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“…[1][2][3] In each case, the authors of those publications have respectfully disagreed with Dr Finkelstein's assertions, although he has since repeated the same claims. [4][5][6] We now would like to respond to his commentary that addresses statements we made in our publication regarding spontaneous mesothelioma in North American women. 7,8 Dr Finkelstein questions 2 statements in our article, both in reference to spontaneous mesothelioma.…”

Section: In Reply To ''Malignant Mesothelioma and Its Nonasbestos Caumentioning

confidence: 99%

“…Although the PlateletMapping test can be used for the assessment of platelet reactivity in response to medication, such as in the recent CREA-TIVE trial, 3 a lot, if not most, of its use is in surgeries with high bleeding risk, such as cardiovascular and trauma surgery. [4][5][6][7][8][9] This is important to note because the clinical reality of this test is much more heterogeneous than that of other tests that are targeted specifically at the platelet effects of certain drugs (mostly P2Y12 inhibitors). Some of the other tests described in this article present with more than 40 000 data points and more than a decade of experience.…”

Section: External Quality Assurance Of Platelet Function Assays: Resumentioning

confidence: 99%

In Reply to “Malignant Mesothelioma and Its Nonasbestos Causes”

Attanoos

Churg

Galateau-Salle

et al. 2019

Archives of Pathology &Amp; Laboratory Medicine

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Response to letters regarding “Cosmetic talc as a risk factor for pleural mesothelioma: a weight of evidence evaluation of the epidemiology”

Cited by 4 publications

References 19 publications

The Effects of Chronic Exposure to Ambient Traffic-Related Air Pollution on Alzheimer’s Disease Phenotypes in Wildtype and Genetically Predisposed Male and Female Rats

The Effects of Chronic Exposure to Ambient Traffic-Related Air Pollution on Alzheimer’s Disease Phenotypes in Wildtype and Genetically Predisposed Male and Female Rats

The effect of exposure time and concentration of airborne PM2.5 on lung injury in mice: A transcriptome analysis

In Reply to “Malignant Mesothelioma and Its Nonasbestos Causes”

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