M I Luster

Centers for Disease Control and Prevention, Druid Hills, GA, United States

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Publications (277)939.67 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: To investigate the association between single nucleotide polymorphisms (SNPs) located across the major histocompatibility complex and susceptibility to diisocyanate-induced asthma (DA). The study population consisted of 140 diisocyanate-exposed workers. Genotyping was performed using the Illumina GoldenGate major histocompatibility complex panels. The HLA-E rs1573294 and HLA-DPB1 rs928976 SNPs were associated with an increased risk of DA under dominant (odds ratio [OR], 6.27; 95% confidence interval [CI], 2.37 to 16.6; OR, 2.79, 95% CI, 0.99 to 7.81, respectively) and recessive genetic models (OR, 6.27, 95% CI, 1.63 to 24.13; OR, 10.10, 95% CI, 3.16 to 32.33, respectively). The HLA-B rs1811197, HLA-DOA rs3128935, and HLA-DQA2 rs7773955 SNPs conferred an increased risk of DA in a dominant model (OR, 7.64, 95% CI, 2.25 to 26.00; OR, 19.69, 95% CI, 2.89 to 135.25; OR, 8.43, 95% CI, 3.03 to 23.48, respectively). These results suggest that genetic variations within HLA genes play a role in DA risk.
    Journal of occupational and environmental medicine / American College of Occupational and Environmental Medicine 04/2014; 56(4):382-7. · 1.88 Impact Factor
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    ABSTRACT: The influence of genetic variability within the major histocompatibility complex (MHC) region on variations in immune responses to childhood vaccination was investigated. The study group consisted of 135 healthy infants who had been immunized with hepatitis B (HBV), 7-valent pneumococcal conjugate (PCV7), and diphtheria, tetanus, acellular pertussis (DTaP) vaccines according to standard childhood immunization schedules. Genotype analysis was performed on genomic DNA using Illumina Goldengate MHC panels (Mapping and Exon Centric). At the 1 year post vaccination check-up total, isotypic, and antigen-specific serum antibody levels were measured using multiplex immunoassays. A number of single nucleotide polymorphisms (SNPs) within MHC Class I and II genes were found to be associated with variations in the vaccine specific antibody responses and serum levels of immunoglobulins (IgG, IgM) and IgG isotypes (IgG1, IgG4) (all at p<0.001). Linkage disequilibrium patterns and functional annotations showed that significant SNPs were strongly correlated with other functional regulatory SNPs. These SNPs were found to regulate the expression of a group of genes involved in antigen processing and presentation including HLA-A, HLA-C, HLA-G, HLA-H, HLA-DRA, HLA-DRB1, HLA-DRB5, HLA-DQA1, HLA-DQB1, HLA-DOB, and TAP-2. The results suggest that genetic variations within particular MHC genes can influence immune response to common childhood vaccinations, which in turn may influence vaccine efficacy.
    Vaccine 09/2013; · 3.77 Impact Factor
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    ABSTRACT: Irritant hand dermatitis (IHD) is common in health care workers. We studied endogenous irritant contact dermatitis threshold by patch testing and exogenous factors such as season and hand washing for their association with IHD in health care workers. Irritant patch testing with sodium lauryl sulfate (SLS), sodium hydroxide, and benzalkonium chloride at varying concentrations was measured in 113 health care workers. Examination for hand dermatitis occurred at 1-month intervals for a period of 6 months in the Midwestern United States. Positive patch testing to low-concentration SLS was associated with IHD (P = 0.0310) after adjusting for age, sex, ethnicity, season, history of childhood flexural dermatitis, mean indoor relative humidity, and glove and hand sanitizer usage. Subjects with a positive patch test to SLS were 78% more likely to have occurrence of IHD (incidence rate ratio [IRR] = 1.78; 95% confidence interval [CI], 0.92-3.45). Hand washing frequency (≥10 times a day; IRR = 1.55; 95% CI, 1.01-2.39) and cold season (IRR = 2.76; 95% CI, 1.35-5.65) were associated with IHD. No association was found between history of childhood flexural dermatitis and IHD in this population. Both genetic and environmental factors are important in the etiology of IHD and should be considered in designing strategies to protect, educate, and treat susceptible individuals.
    Dermatitis 07/2013; 24(4):170-5. · 0.93 Impact Factor
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    ABSTRACT: The Immunotoxicology Specialty Section of the Society of Toxicology (SOT) celebrated the 50(th) Anniversary of the SOT by constructing a poster to highlight the milestones of Immunotoxicology during that half-century period. This poster was assembled by an ad hoc committee and intertwines in words, citations, graphics, and photographs our attempts to capture a timeline reference of the development and progressive movement of immunotoxicology across the globe. This poster was displayed during the 50(th) Annual SOT Meeting in Washington DC in March, 2011. The poster can be accessed by any Reader at the SOT Website via the link http://www.toxicology.org/AI/MEET/AM2011/posters_rcsigss.asp#imss. We dedicate this poster to all of the founders and the scientists that followed them who have made the discipline of Immunotoxicology what it is today.
    Journal of Immunotoxicology 10/2012; · 1.57 Impact Factor
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    ABSTRACT: Recently, a genome wide association study (GWAS) conducted in Korean subjects identified three CTNNA3 (alpha-T catenin) single nucleotide polymorphisms (SNPs) (rs10762058, rs7088181, and rs4378283) associated with diisocyanate induced occupational asthma (DA). The CTNNA3 gene codes for a cadherin involved in formation of stretch-resistant cell-cell adhesions. We conducted a candidate gene association study to replicate these findings in Caucasian workers. Genotyping was performed on DNA using a 5' nuclease PCR assay collected from 410 diisocyanate exposed and predominantly Canadian workers including: 132 workers with DA confirmed by a specific inhalation challenge (DA+); 131 symptomatic workers in whom DA was excluded by a negative challenge (DA-); and 147 HDI-exposed asymptomatic workers (AWs). As in the Korean study, highly linked CTNNA3 rs7088181 and rs10762058 SNPs were significantly associated with DA+ when compared to AWs but not in comparison to DA- workers (p≤ 0.05). After adjusting for potentially confounding variables of age, smoking status and duration of exposure, minor allele homozygotes of rs7088181 and rs10762058 SNPs were at increased risk for DA compared with AWs [OR= 9.05 (95% CI:1.69, 48.54) and OR = 6.82 (95% CI:1.65, 28.24), respectively]. In conclusion, we replicated results from the only reported GWAS study of DA demonstrating an association between two closely linked CTNNA3 gene SNPs and DA. These findings lend further support to the clinical relevance of these genotypes in predicting susceptibility to DA and the potential importance of cadherins in the disease process.
    Toxicological Sciences 09/2012; · 4.33 Impact Factor
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    ABSTRACT: Diisocyanates are a common cause of occupational asthma, but risk factors are not well defined. A case-control study was conducted to investigate whether genetic variants of antioxidant defense genes, glutathione S-transferases (GSTM1, GSTT1, GSTM3, GSTP1), manganese superoxide dismutase (SOD2), and microsomal epoxide hydrolase (EPHX1) are associated with increased susceptibility to diisocyanate-induced asthma (DA). The main study population consisted of 353 Caucasian French-Canadians from among a larger sample of 410 diisocyanate-exposed workers in three groups: workers with specific inhalation challenge (SIC) confirmed DA (DA(+), n = 95); symptomatic diisocyanate workers with a negative SIC (DA(-), n = 116); and asymptomatic exposed workers (AW, n = 142). Genotyping was performed on genomic DNA, using a 5'-nuclease PCR assay. The SOD2 rs4880, GSTP1 rs1695, and EPHX1 rs2740171 variants were significantly associated with DA in both univariate and multivariate analyses. In the first logistic regression model comparing DA(+) and DA(-) groups, SOD2 rs4880, GSTM1 (null), GSTP1 rs762803, and EPHX1 rs2854450 variants were associated with DA (p = 0.004, p = 0.047, p = 0.021, p <0.001, respectively). Genotype combinations GSTT1*GSTP1 rs762803, GSTM1*EPHX1 rs2854450, EPHX1 rs2740168*EPHX1 rs1051741, and GSTP1 rs762803*EPHX1 rs2740168 were also associated with DA in this model (p = 0.027, p = 0.002, p = 0.045, p = 0.044, respectively). The GSTP1 rs1695 and EPHX1 rs1051741 and rs2740171 variants showed an association with DA in the second model comparing DA(+) and AW groups (p = 0.040, p = 0.019, p = 0.002, respectively). The GSTM3 rs110913*EPHX1 rs1051741 genotype combination was also associated with DA under this model (p = 0.042). The results suggest that variations in SOD2, GST, and EPHX1 genes and their interactions contribute to DA susceptibility.
    Toxicological Sciences 05/2012; 129(1):166-73. · 4.33 Impact Factor
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    The Journal of allergy and clinical immunology 04/2011; 128(2):418-20. · 12.05 Impact Factor
  • Journal of Allergy and Clinical Immunology - J ALLERG CLIN IMMUNOL. 01/2010; 125(2).
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    ABSTRACT: The magnitude of the immune response to vaccinations can be influenced by genetic variability. In the present study, we aimed to investigate whether cytokine or cytokine receptor gene polymorphisms were associated with variations in the immune response to childhood vaccination. The study group consisted of 141 healthy infants who had been immunized with hepatitis B vaccine (HBV), 7-valent pneumococcal conjugate (PCV7), and diphtheria, tetanus, acellular pertussis (DTaP) vaccines according to standard childhood immunization schedules. Genotype analysis was performed on genomic DNA using a 5' nuclease PCR assay. Post vaccination total, isotypic, and antigen-specific serum antibody levels were measured using multiplex immunoassays. Significant associations were observed between SNPs in the TNFalpha, IL-12B, IL-4Ralpha, and IL-10 genes and vaccine-specific immune responses (p<0.05). In addition, SNPs in the IL-1beta, TNFalpha, IL-2, IL-4, IL-10, IL-4Ralpha, and IL-12B genes were associated with variations in serum levels of immunoglobulins (IgG, IgA, IgM) and IgG isotypes (IgG1-IgG3) (p<0.05). These data suggest that genetic variations in cytokine genes can influence vaccine-induced immune responses in infants, which in turn may influence vaccine efficacy.
    Vaccine 10/2009; 27(50):6991-7. · 3.77 Impact Factor
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    ABSTRACT: The purpose of this study was to investigate whether the expression of specific genes in peripheral blood can be used as surrogate marker(s) to detect and distinguish target organ toxicity induced by chemicals in rats. Rats were intraperitoneally administered a single, acute dose of a well-established hepatotoxic (acetaminophen) or a neurotoxic (methyl parathion) chemical. Administration of acetaminophen (AP) in the rats resulted in hepatotoxicity as evidenced from elevated blood transaminase activities. Similarly, administration of methyl parathion (MP) resulted in neurotoxicity in the rats as evidenced from the inhibition of acetyl cholinesterase activity in their blood. Administration of either chemical also resulted in mild hematotoxicity in the rats. Microarray analysis of the global gene expression profile of rat blood identified distinct gene expression markers capable of detecting and distinguishing hepatotoxicity and neurotoxicity induced by AP and MP, respectively. Differential expressions of the marker genes for hepatotoxicity and neurotoxicity were detectable in the blood earlier than the appearance of the commonly used clinical markers (serum transaminases and acetyl cholinesterase). The ability of the marker genes to detect hepatotoxicity and neurotoxicity was further confirmed using the blood samples of rats administered additional hepatotoxic (thioacetamide, dimethylnitrobenzene, and carbon tetrachloride) or neurotoxic (ethyl parathion and malathion) chemicals. In summary, our results demonstrated that blood gene expression markers can detect and distinguish target organ toxicity non-invasively.
    Molecular and Cellular Biochemistry 09/2009; 335(1-2):223-34. · 2.33 Impact Factor
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    ABSTRACT: Assessing adverse effects from environmental chemical exposure is integral to public health policies. Toxicology assays identifying early biological changes from chemical exposure are increasing our ability to evaluate links between early biological disturbances and subsequent overt downstream effects. A workshop was held to consider how the resulting data inform consideration of an "adverse effect" in the context of hazard identification and risk assessment. Our objective here is to review what is known about the relationships between chemical exposure, early biological effects (upstream events), and later overt effects (downstream events) through three case studies (thyroid hormone disruption, antiandrogen effects, immune system disruption) and to consider how to evaluate hazard and risk when early biological effect data are available. Each case study presents data on the toxicity pathways linking early biological perturbations with downstream overt effects. Case studies also emphasize several factors that can influence risk of overt disease as a result from early biological perturbations, including background chemical exposures, underlying individual biological processes, and disease susceptibility. Certain effects resulting from exposure during periods of sensitivity may be irreversible. A chemical can act through multiple modes of action, resulting in similar or different overt effects. For certain classes of early perturbations, sufficient information on the disease process is known, so hazard and quantitative risk assessment can proceed using information on upstream biological perturbations. Upstream data will support improved approaches for considering developmental stage, background exposures, disease status, and other factors important to assessing hazard and risk for the whole population.
    Environmental Health Perspectives 12/2008; 116(11):1568-75. · 7.26 Impact Factor
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    ABSTRACT: Perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS) are environmentally widespread and persistent chemicals with multiple toxicities reported in experimental animals and humans. These compounds can trigger biological activity by activating the alpha isotype of peroxisome proliferator-activated receptors (PPARs), ligand-activated transcription factors that regulate gene expression; however, some biological effects may occur independently of the receptor. Activation of the peroxisome proliferator-activated receptor alpha (PPARalpha) modulates lipid and glucose homeostasis, cell proliferation and differentiation, and inflammation. Reported immunomodulation in experimental animals exposed to PFOA and PFOS has included altered inflammatory responses, production of cytokines and other proteins, reduced lymphoid organ weights, and altered antibody synthesis. Mounting experimental animal evidence suggests PPARalpha independence of some immune effects. This evidence originates primarily from studies with PPARalpha knockout models exposed to PFOA that demonstrate hepatic peroxisome proliferation, reduced lymphoid organ weights, and altered antibody synthesis. As human PPARalpha expression is significantly less than that of rodents, potential PPARalpha independence indicates that future research must explore mechanisms of action of these compounds, including PPARalpha-dependent and -independent pathways. This multiauthored review contains brief descriptions of current and recently published work exploring immunomodulation by PFOA and PFOS, as well as a short overview of other PPARalpha ligands of therapeutic and environmental interest.
    Critical Reviews in Toxicology 10/2008; 39(1):76-94. · 6.25 Impact Factor
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    ABSTRACT: To investigate whether genetic variants involved in cytokine expression are associated with the age-related rate of decline in forced expiratory volume in 1 second (FEV1). Functional polymorphisms in the TNFalpha, TGF beta 1, IL-1 beta, IL-1RN, IL-13, and IL-8 genes were investigated in 374 active firefighters with at least five pulmonary function tests. A protective effect was found between the presence of the TGF beta 1 -509 TT genotype and rate of decline in FEV1 (P = 0.043). Carrying an A allele at TNFalpha -308 (P = 0.010) and GG genotype at TNFalpha -238 (P = 0.028) was associated with a more rapid rate of FEV1 decline. The TNFalpha -308A/-238G haplotype was also associated with an increased rate of decline as compared with the other haplotypes. Interindividual variability in progressive decline in FEV1 may be explained in part by genetic variations within genes involved in inflammatory responses.
    Journal of occupational and environmental medicine / American College of Occupational and Environmental Medicine 07/2008; 50(6):642-8. · 1.88 Impact Factor
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    ABSTRACT: Progressive massive fibrosis (PMF) is a chronic interstitial lung disease with a complex aetiology that can occur after cumulative dust exposure. A case-control study was conducted to test the hypothesis that single nucleotide polymorphisms (SNPs) within genes involved in inflammatory and fibrotic processes modulate the risk of PMF development. The study population consisted of 648 underground coal miners participating in the National Coal Workers Autopsy Study, of which 304 were diagnosed with PMF. SNPs that influence the regulation of interleukin (IL)-1, IL-6, tumour necrosis factor-alpha, transforming growth factor-beta1, vascular endothelial growth factor (VEGF), epidermal growth factor intercellular cell adhesion molecule (ICAM)-1 and matrix metalloproteinase-2 genes were determined using a 5'-nuclease real-time PCR assay. There were no significant differences in the distribution of any individual SNP or haplotype between the PMF and control groups. However, the polygenotype of VEGF +405/ICAM-1 +241/IL-6 -174 (C-A-G) conferred an increased risk for PMF (odds ratio 3.4, 95% confidence interval 1.3-8.8). The present study suggests that the examined genetic variations that help regulate inflammatory and fibrotic processes are unlikely to strongly influence susceptibility to this interstitial lung disease, although the role of vascular endothelial growth factor, intercellular cell adhesion molecule-1 and interleukin-6 polymorphisms in the development of progressive massive fibrosis may require further investigation.
    European Respiratory Journal 07/2008; 31(6):1177-82. · 6.36 Impact Factor
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    ABSTRACT: Cytokines are polypeptide mediators produced by a variety of cell types that play crucial roles in immune and inflammatory responses. Genes that code for cytokines are highly polymorphic, and some of these polymorphisms directly or indirectly influence cytokine expression. The most frequent types of mutations are characterized by a change in a single nucleotide base pair and are called single nucleotide polymorphisms (SNPs). Many SNPs that affect cytokine expression represent disease modifiers and influence the severity or progression of immune-mediated and chronic inflammatory diseases. SNPs in cytokine genes have been associated with common diseases, including cardiovascular diseases, cancer, neurodegenerative diseases, allergy, and asthma, and data are now accumulating on their role in occupational/environmental diseases. All these diseases are multigenic and multifactorial in nature and involve interactions between genetic, physiological, and environmental factors. Currently, there exist inconsistencies in association studies examining relationships between cytokine SNPs and disease because of known limitations in population-based studies. Recent advances in geno typing platforms for largescale genetic studies, more robust study designs, and haplotype analysis should help reduce the amount of spurious and inconsistent associations in the literature and allow for incorporating genetic information into the risk assessment process although challenges still remain. Key WordsCytokine–polymorphism–SNP–common diseases–autoimmune diseases–occupational diseases–epidemiology
    06/2008: pages 113-132;
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    ABSTRACT: Reactivation of latent herpes virus has been linked to triggers of mild immunosupression, such as stress or UV-exposure. Despite having predictive value in severe immunodeficiency, the white blood cell (WBC) differential count has not been examined in relation to risk of herpes reactivation in population studies. The WBC differential count and other risk factors for herpes labialis were examined in 5687 adults (ages 18-64) from the Third National Health and Nutrition Examination Survey, who had WBC 3.5-11 x 10(6) cells mL(-1) and reported no acute infections in the past month. The association between self-reported herpes labialis in the past year and the WBC differential count was modeled, adjusting for age, sex, race/ethnicity, education, smoking, upper respiratory infections (URI), and HSV-1 antibodies. Herpes labialis was significantly associated with white race/ethnicity, being a nonsmoker, and frequent URI. Compared with the highest quartile, being in the lowest quartile of granulocytes was associated with herpes labialis, adjusted odds ratio=1.82 (95% confidence interval 1.20, 2.28). At the same time, there was a trend towards an inverse association of lower lymphocyte count and herpes labialis. These findings suggest that moderate differences in the WBC differential count are related to reactivation of HSV-1. Prospective studies may help to show whether such differences indicate susceptibility to loss of latency or represent a consequence of reactivated infection.
    FEMS Immunology & Medical Microbiology 12/2007; 51(2):336-43. · 2.68 Impact Factor
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    ABSTRACT: The transforming growth factor-beta1 (TGF-beta1) is involved in post-ischemic neuronal rescue and in beta-amyloid turn-over. We hypothesized that the risk for dementia and related neuropathologies is modified by the TGF-beta1 functional genetic variants. The association of the TGF-beta1+29T-->C polymorphism with dementia was examined in a sample of 261 cases and 491 controls from the Honolulu-Asia Aging Study, including 282 subjects with autopsy data. Dementia was assessed in 1991 and 1994 by a multi-step protocol and standardized diagnostic criteria. The analysis was adjusted for demographic and vascular factors. Compared to the TT genotype, the TC and the CC genotypes were associated with a reduced risk for vascular dementia (OR(TC)=0.28, 95% confidence interval (CI): 0.1-0.9; OR(CC)=0.28, CI: 0.1-0.9), microinfarcts (OR(CC)=0.31, CI: 0.13-0.71) and cerebral amyloid angiopathy (OR(CC)=0.48, CI: 0.2-0.9). The CC genotype was associated with an increase risk of neocortical plaques (OR(CC)=4.34, CI: 1.6-11.8). These preliminary data suggest that the TGF genetic variability may be important in the risk of vascular related dementia.
    Neurobiology of aging 10/2007; 28(9):1367-73. · 5.94 Impact Factor
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    ABSTRACT: Diisocyanates are the leading cause of occupational asthma, and epidemiological evidence suggests that occupational rhinitis is a comorbid and preceding condition in patients who develop asthma. The goal of the present studies was to develop and characterize a murine model of toluene diisocyanate (TDI)-induced rhinitis. Female C57BL/6 mice were exposed to workplace-relevant concentrations of TDI vapor via inhalation for 4 h/day for 12 days with or without a 2-wk rest period and TDI challenge. Mice exposed 12 consecutive weekdays to 50 parts per billion TDI vapor showed elevated total serum IgE and increased TDI-specific IgG titers. Breathing rates were decreased corresponding with increased inspiratory time. TDI exposure elevated IL-4, IL-5, IL-13, and IFN-gamma mRNA expression in the nasal mucosa, suggesting a mixed Th1/Th2 immune response. Expressions of mRNA for proinflammatory cytokines and adhesion molecules were also up-regulated. These cytokine changes corresponded with a marked influx of inflammatory cells into the nasal mucosa, eosinophils being the predominant cell type. Removal from exposure for 2 wk resulted in reduced Ab production, cytokine mRNA expression, and cellular inflammation. Subsequent challenge with 50 parts per billion TDI vapor resulted in robust up-regulation of Ab production, cytokine gene expression, as well as eosinophilic inflammation in the nasal mucosa. There were no associated changes in the lung. The present model shows that TDI inhalation induces immune-mediated allergic rhinitis, displaying the major features observed in human disease. Future studies will use this model to define disease mechanisms and examine the temporal/dose relationship between TDI-induced rhinitis and asthma.
    The Journal of Immunology 09/2007; 179(3):1864-71. · 5.52 Impact Factor
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    ABSTRACT: There is increasing evidence that obesity and overweight may be related, in part, to adverse work conditions. In particular, the risk of obesity may increase in high-demand, low-control work environments, and for those who work long hours. In addition, obesity may modify the risk for vibration-induced injury and certain occupational musculoskeletal disorders. We hypothesized that obesity may also be a co-risk factor for the development of occupational asthma and cardiovascular disease that and it may modify the worker's response to occupational stress, immune response to chemical exposures, and risk of disease from occupational neurotoxins. We developed 5 conceptual models of the interrelationship of work, obesity, and occupational safety and health and highlighted the ethical, legal, and social issues related to fuller consideration of obesity's role in occupational health and safety.
    American Journal of Public Health 04/2007; 97(3):428-36. · 3.93 Impact Factor
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    ABSTRACT: Engineered nanosized materials, such as single-wall carbon nanotubes (SWCNT), are emerging as technologically important in different industries. The unique physical characteristics and the pulmonary toxicity of SWCNTs raised concerns that respiratory exposure to these materials may be associated with cardiovascular adverse effects. In these studies we evaluated aortic mitochondrial alterations by oxidative stress assays, including quantitative polymerase chain reaction of mitochondrial (mt) DNA and plaque formation by morphometric analysis in mice exposed to SWCNTs. A single intrapharyngeal instillation of SWCNTs induced activation of heme oxygenase-1 (HO-1), a marker of oxidative insults, in lung, aorta, and heart tissue in HO-1 reporter transgenic mice. Furthermore, we found that C57BL/6 mice, exposed to SWCNT (10 and 40 mug/mouse), developed aortic mtDNA damage at 7, 28, and 60 days after exposure. mtDNA damage was accompanied by changes in aortic mitochondrial glutathione and protein carbonyl levels. Because these modifications have been related to cardiovascular diseases, we evaluated whether repeated exposure to SWCNTs (20 mug/mouse once every other week for 8 weeks) stimulates the progression of atherosclerosis in ApoE(-/-) transgenic mice. Although SWCNT exposure did not modify the lipid profiles of these mice, it resulted in accelerated plaque formation in ApoE(-/-) mice fed an atherogenic diet. Plaque areas in the aortas, measured by the en face method, and in the brachiocephalic arteries, measured histopathologically, were significantly increased in the SWCNT-treated mice. This response was accompanied by increased mtDNA damage but not inflammation. Taken together, the findings are of sufficient significance to warrant further studies to evaluate the systemic effects of SWCNT under workplace or environmental exposure paradigms.
    Environmental Health Perspectives 04/2007; 115(3):377-82. · 7.26 Impact Factor

Publication Stats

7k Citations
939.67 Total Impact Points

Institutions

  • 1999–2009
    • Centers for Disease Control and Prevention
      • Health Effects Laboratory Division
      Druid Hills, GA, United States
  • 2008
    • East Carolina University
      North Carolina, United States
  • 2007
    • Molecular Toxicology, Inc.
      North Carolina, United States
    • National Institute on Aging
      • Laboratory of Epidemiology, Demography and Biometry (LEDB)
      Baltimore, MD, United States
  • 2006
    • United States Environmental Protection Agency
      • Office of Research and Development
      Washington, D. C., DC, United States
  • 2005
    • ILSI Health and Environmental Sciences Institute
      Washington, Washington, D.C., United States
  • 1979–2005
    • National Institute of Environmental Health Sciences
      Durham, North Carolina, United States
  • 2004
    • Centers for Disease Control, Lesotho
      Maseru, Maseru, Lesotho
  • 2003
    • National Institute for Public Health and the Environment (RIVM)
      • Laboratory for Health Protection Research
      Utrecht, Utrecht, Netherlands
  • 2002–2003
    • Ankara University
      • Faculty of Pharmacy
      Ankara, Ankara, Turkey
    • Georgia State University
      • Division of Physical Therapy
      Atlanta, GA, United States
  • 2001
    • National Institute of Occupational Safety and Health JAPAN
      Edo, Tōkyō, Japan
  • 1986–1999
    • University of North Carolina at Chapel Hill
      • Department of Pharmacology
      Chapel Hill, NC, United States
  • 1978–1999
    • National Institutes of Health
      • Laboratory of Experimental Immunology
      Bethesda, MD, United States
  • 1994–1996
    • Virginia Polytechnic Institute and State University
      • Department of Biomedical Sciences and Pathobiology
      Blacksburg, VA, United States
  • 1990–1991
    • Virginia Commonwealth University
      • Department of Pharmacology and Toxicology
      Richmond, VA, United States