Occupational Health science Institute
Occupational Health science Institute
Hossain M.M.,Occupational Health science Institute |
Hossain M.M.,Northeast Ohio Medical University |
Liu J.,Occupational Health science Institute |
Richardson J.R.,Occupational Health science Institute |
Richardson J.R.,Northeast Ohio Medical University
Toxicological Sciences | Year: 2017
Microglia are considered to be the resident immune cells of the central nervous system and contribute significantly to ongoing neuroinflammation in a variety of neurodegenerative diseases. Recently, we and others identified that voltagegated sodium channels (VGSC) are present on microglia cells and contribute to excessive accumulation of intracellular Na+ and release of major pro-inflammatory cytokine tumor necrosis factor alpha (TNF-α). Based on this finding and the fact that pyrethroid pesticides act on VGSC, we hypothesized that exposure of microglia to the pyrethroid pesticides, permethrin and deltamethrin, would activate microglia and increase the release of TNF-α. BV2 cells or primary microglia were treated with 0-5 μM deltamethrin or permethrin in the presence or absence of tetrodotoxin (TTX), a VGSC blocker for 24-48 h. Both pyrethroids caused a rapid Na+ influx and increased accumulation of intracellular sodium [(Na+)i] in the microglia in a dose- and time-dependent manner, which was significantly reduced by TTX. Furthermore, deltamethrin and permethrin increased the release of TNF-α in a dose- and time-dependent manner, which was significantly reduced by pretreatment of cells with TTX. These results demonstrate that pyrethroid pesticides may directly activate microglial cells through their interaction with microglial VGSC. Because neuroinflammation plays a key role in many neurodegenerative diseases, these data provide an additional mechanism by which exposure to pyrethroid insecticides may contribute to neurodegeneration. © The Author 2016. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved.
Yu C.H.,Occupational Health science Institute |
Black K.,Occupational Health science Institute |
Lin L.,Occupational Health science Institute |
Lioy P.J.,Occupational Health science Institute |
And 2 more authors.
Science of the Total Environment | Year: 2010
In contrast to Cr+3, Cr+6 is carcinogenic and allergenic. Although Cr+6 can occur naturally, it is thought that most soil Cr+6 is anthropogenic, however, the extent of Cr+6 in the background environment is unknown. Cr+6-containing chromite ore processing residue (COPR) from chromate manufacture was deposited in numerous locations in Jersey City (JC), New Jersey. In the 1990's, significantly elevated concentrations of total Cr (Cr+6+Cr+3) were found in house dust near COPR sites. We undertook a follow-up study to determine ongoing COPR exposure. We compared Cr+6 in house dust in JC to selected background communities with no known sources of Cr+6. Samples were collected from living areas, basements and window wells. Cr+6 was detected in dust from all JC and background houses. In the JC homes, the mean (±SD) Cr+6 concentration for all samples was 3.9±7.0μg/g (range: non-detect-90.4μg/g), and the mean Cr+6 loading was 5.8±15.7μg/m2 (range: non-detect-196.4μg/m2). In background homes, the mean Cr+6 concentrations of all samples was 4.6±7.8μg/g, (range, 0.05-56.6μg/g). The mean loading was 10.0±27.9μg/m2 (range, 0.22-169.3μg/m2). There was no significant difference between Cr+6 dust concentrations in Jersey City and background locations. Stratification by sample location within houses and sampling method gave similar results. Samples exceeding 20μg/g were obtained only from single wood surfaces in different homes. Lower concentrations in window well samples suggests transport from outside is not the major source of indoor Cr+6. Landscaping and groundcover may influence indoor Cr+6. There appears to be a widespread low level background of Cr+6 that is not elevated in Jersey City homes despite its historic COPR contamination. It is possible that house dust, in general, is a source of Cr+6 exposure with potential implications for persistence of chromium allergic contact dermatitis. © 2010 Elsevier B.V.