Beach Related Illness - Left the Key Data Out of the Abstract

BrooklynDodger(s) comment: The most interesting number, the overall rate of illnesses, never made the abstract, only the risk ratios. So it's a 20% increase, but 20% of what?


American Journal of Epidemiology 2009 170(2):164-172; doi:10.1093/aje/kwp152

Contact With Beach Sand Among Beachgoers and Risk of Illness

Christopher D. Heaney, Elizabeth Sams, Steve Wing, Steve Marshall, Kristen Brenner, Alfred P. Dufour and Timothy J. Wade

Correspondence to Dr. Christopher D. Heaney, Campus Box 7435, Department of Epidemiology, University of North Carolina, Chapel Hill, NC 27599-7435 (e-mail: cheaney@email.unc.edu).

Received for publication February 2, 2009. Accepted for publication May 6, 2009.

Recent studies of beach sand fecal contamination have triggered interest among scientists and in the media. Although evidence shows that beach sand can harbor high concentrations of fecal indicator organisms, as well as fecal pathogens, illness risk associated with beach sand contact is not well understood. Beach visitors at 7 US beaches were enrolled in the National Epidemiological and Environmental Assessment of Recreational Water (NEEAR) Study during 2003–2005 and 2007 and asked about sand contact on the day of their visit to the beach (digging in the sand, body buried in the sand). Then, 10–12 days after their visit, participants were telephoned to answer questions about any health symptoms experienced since the visit. The authors completed 27,365 interviews. Digging in the sand was positively associated with gastrointestinal illness (adjusted incidence proportion ratio (aIPR) = 1.13, 95% confidence interval (CI): 1.02, 1.25) and diarrhea (aIPR = 1.20, 95% CI: 1.05, 1.36). The association was stronger between those buried in the sand and gastrointestinal illness (aIPR = 1.23, 95% CI: 1.05, 1.43) and diarrhea (aIPR = 1.24, 95% CI: 1.01, 1.52). Nonenteric illnesses did not show a consistent association with sand contact activities. Sand contact activities were associated with enteric illness at beach sites. Variation in beach-specific results suggests that site-specific factors may be important in the risk of illness following sand exposure.

bathing beaches; diarrhea; disease transmission, infectious; environmental pollution; fomites; fresh water; oceans and seas; sewage

Tall is a Risk Factor

BrooklynDodger(s) comment: There's a lot of literature that being big is associated with increased risks of cancer. No one knows why. The concluding sentence is pretty weak.


American Journal of Epidemiology 2009 170(3):297-307; doi:10.1093/aje/kwp12

Body Mass Index, Height, and Risk of Lymphatic Malignancies: A Prospective Cohort Study

Romana D. Pylypchuk, Leo J. Schouten, R. Alexandra Goldbohm, Harry C. Schouten and Piet A. van den Brandt

Correspondence to Dr. Leo J. Schouten, Department of Epidemiology, GROW-School for Oncology and Developmental Biology, Maastricht University, P.O. Box 616, 6200 MD Maastricht, the Netherlands (e-mail: lj.schouten@epid.unimaas.nl).

Received for publication December 1, 2008. Accepted for publication April 23, 2009.

The association among body mass index (BMI), height, and the risk of lymphatic malignancies was investigated in the Netherlands Cohort Study. The participants (n = 120,852), Dutch men and women aged 55–69 years, completed a self-administered questionnaire at baseline in 1986. After 13.3 years of follow-up, data on 1,042 lymphatic malignancy cases (including diffuse large-cell lymphoma, chronic lymphocytic leukemia, multiple myeloma, and other subtypes) and 4,588 subcohort members were available. Incidence rate ratios were estimated by using Cox regression models. BMI at baseline and BMI change since the age of 20 years were not associated with lymphatic malignancy risk. However, the rate ratio of lymphatic malignancies per 4-unit increase in BMI at 20 years of age was 1.13 (95% confidence interval (CI): 1.01, 1.25). The rate ratio of lymphatic malignancies per 5-cm increase in height was 1.08 (95% CI: 1.02, 1.15). For diffuse large-cell lymphoma, follicular lymphoma, and chronic lymphocytic leukemia, the relative risks were 1.19 (95% CI: 1.07, 1.33), 1.15 (95% CI: 0.95, 1.40), and 1.09 (95% CI: 0.95, 1.26), respectively, for each 5-cm increase in height. The positive associations among BMI at 20 years of age, height, and the risk of lymphatic malignancies suggest that exposures during early life play a role in the etiology of lymphatic malignancies.

anthropometry; body height; body mass index; leukemia, lymphocytic, chronic, B-cell; lymphoma, non-Hodgkin; lymphoproliferative disorders; multiple myeloma

BrooklynDodger(s) comments: A bunch of endpoints the Dodger(s) has(have) never heard of. An effect level for an ignored male organ.


Toxicology
Volume 262, Issue 3, 21 August 2009, Pages 215-223

Long-term effects of developmental exposure to di-n-butyl-phthalate (DBP) on rat prostate: Proliferative and inflammatory disorders and a possible role of androgens

References and further reading may be available for this article. To view references and further reading you must purchase this article.

Wellerson Rodrigo Scarano^{a, ,} , Fabíola Choqueta de Toledo^b, Marina Trevizan Guerra^a, Silvana Gisele Pegorin de Campos^c, Luís Antonio Justulin Júnior^b, Sérgio Luis Felisbino^a, Janete A. Anselmo-Franci^d, Sebastião Roberto Taboga^c and Wilma De Grava Kempinas^a

^aDepartment of Morphology, Institute of Biosciences, UNESP, Botucatu, SP, 18618-000, Brazil

^bGraduate Program in Cellular and Structural Biology, Institute of Biology, State University of Campinas, UNICAMP, 13083-970, Brazil

^cDepartment of Biology, Institute of Biosciences, Humanities and Exact Sciences (IBILCE), UNESP, São José do Rio Preto, SP, 15100-000, Brazil

^dDepartment of Morphology, Stomatology and Physiology, School of Dentistry, University of São Paulo, USP, Ribeirão Preto, SP, Brazil

Abstract

In the present study we evaluated the toxic effects on the male adult rat prostate of DBP exposure during fetal and lactational periods, because although many studies have addressed the influence of phthalates on the male reproductive system, only a few have discussed their possible effects on prostate development. Pregnant females were distributed into two experimental groups: Control (C) and Treated (T). The females of the T group received DBP (100 mg/kg, by gavage) from gestation day 12 to postnatal day 21, while C rats received the vehicle (corn oil). In adulthood (90 days old), the animals were euthanized. The serum and testicular testosterone levels were measured. Ventral prostate was removed and weighed. Distal segment fragments of the ventral prostate were fixed and processed for histochemistry and immunohistochemistry to detect androgen receptor (AR) and Ki67 antigens. Protein extraction from ventral prostate fragments was performed for AR immunoblotting and Gelatin zymography for MMP-2 and MMP-9 (MMP, metalloproteinase). Stereological and histopathological analyses were also performed. Serum and testicular testosterone levels and prostate weight were comparable between groups. In the T group the relative proportions (%) of epithelial (C = 32.86; T = 42.04*) and stromal (C = 21.61; T = 27.88*) compartments were increased, while the luminal compartment was decreased (C = 45.54; T = 30.08*), *p <>T, disseminated inflammatory infiltrate in the stroma, associated or not with epithelial dysplasia and PIN (Prostatic Intraepithelial Neoplasia), was observed. Increases in AR expression, proliferation index and metalloproteinase 9 (MMP-9) activity were noted in T animals. In some T animals, collagen fibrils accumulated adjacent to the epithelium. As far as we are aware, this is the first report in the literature showing that phthalates could play a role in proliferative and inflammatory disorders of the rat prostate.

Losing Your Marbles with Age

BrooklynDodger(s) comment: Not very informative. Have to read the full text to see what these scored mean.


American Journal of Epidemiology 2009 170(3):331-342; doi:10.1093/aje/kwp154

Trajectories of Cognitive Function in Late Life in the United States: Demographic and Socioeconomic Predictors

Arun S. Karlamangla, Dana Miller-Martinez, Carol S. Aneshensel, Teresa E. Seeman, Richard G. Wight and Joshua Chodosh

Correspondence to Dr. Arun S. Karlamangla, UCLA Division of Geriatrics, 10945 Le Conte Avenue, Suite 2339, Los Angeles, CA 90095 (e-mail: akarlamangla@mednet.ucla.edu).

Received for publication February 11, 2009. Accepted for publication May 11, 2009.

This study used mixed-effects modeling of data from a national sample of 6,476 US adults born before 1924, who were tested 5 times between 1993 and 2002 on word recall, serial 7's, and other mental status items to determine demographic and socioeconomic predictors of trajectories of cognitive function in older Americans. Mean decline with aging in total cognition score (range, 0–35; standard deviation, 6.00) was 4.1 (0.68 standard deviations) per decade (95% confidence interval: 3.8, 4.4) and in recall score (range, 0–20; standard deviation, 3.84) was 2.3 (0.60 standard deviations) per decade (95% confidence interval: 2.1, 2.5). Older cohorts (compared with younger cohorts), women (compared with men), widows/widowers, and those never married (both compared with married individuals) declined faster, and non-Hispanic blacks (compared with non-Hispanic whites) and those in the bottom income quintile (compared with the top quintile) declined slower. Race and income differences in rates of decline were not sufficient to offset larger differences in baseline cognition scores. Educational level was not associated with rate of decline in cognition scores. The authors concluded that ethnic and socioeconomic disparities in cognitive function in older Americans arise primarily from differences in peak cognitive performance achieved earlier in the life course and less from declines in later life.

Depression and the Neighborhood Environment

Epidemiologic Reviews 2008 30(1):101-117; doi:10.1093/epirev/mxn009

Blues from the Neighborhood? Neighborhood Characteristics and Depression

Daniel Kim

From the Department of Society, Human Development, and Health, Harvard School of Public Health, Boston, MA

Correspondence to Dr. Daniel Kim, Department of Society, Human Development, and Health, Harvard School of Public Health, 677 Huntington Avenue, 7th Floor, Boston, MA 02115 (e-mail: dkim@hsph.harvard.edu).

accepted for publication May 22, 2008.

Unipolar major depression ranks among the leading contributors to the global burden of disease. Although established risk factors for depression include a variety of individual-level characteristics, neighborhood etiologic factors have been relatively understudied, with several such attributes (neighborhood socioeconomic status, physical conditions, services/amenities, social capital, social disorder) possessing plausible linkages to depression. Using the PubMed database (1966–2008) and the Social Sciences Citation Index database (1956–2008), the author undertook a systematic review of the published literature on the associations between these characteristics and depression in adults. Across studies, the evidence generally supports harmful effects of social disorder and, to a lesser extent, suggests protective effects for neighborhood socioeconomic status. Few investigations have explored the relations for neighborhood physical conditions, services/amenities, and social capital, and less consistently point to salutary effects. The unsupportive findings may be attributed to the lack of representative studies within and across societies or to methodological gaps, including lack of control for other neighborhood/non-neighborhood exposures and lack of implementation of more rigorous methodological approaches. Establishing mediating pathways and effect-modifying factors will vitally advance understanding of neighborhood effects on depression. Overall, addressing these gaps will help to identify what specific neighborhood features matter for depression, how, and for whom, and will contribute to curtailing the burden of disease associated with this major disorder.

Work Stress Can Make You Crazy

BrooklynDodger(s) comment: The literature may be too big or too small. Over 1000 studies were boiled down to 14. Then, the authors seem to conclude that the 14 were not enough to draw a strong conclusion.

Epidemiologic Reviews 2008 30(1):118-132; doi:10.1093/epirev/mxn004

The Relation between Work-related Psychosocial Factors and the Development of Depression
Bo Netterstrøm1, Nicole Conrad1, Per Bech2, Per Fink3, Ole Olsen4, Reiner Rugulies4 and Stephen Stansfeld5

1 Clinic of Occupational Medicine, Hillerød Hospital, Hillerød, Denmark
2 Psychiatric Research Unit, Hillerød Hospital, Hillerød, Denmark
3 Research Clinic for Functional Disorders, Aarhus University Hospital, Aarhus, Denmark
4 National Research Centre for the Working Environment, Copenhagen, Denmark
5 Centre for Psychiatry, Wolfson Institute of Preventive Medicine, Queen Mary's School of Medicine and Dentistry, London, United Kingdom

Correspondence to Dr. Bo Netterstrøm, Clinic of Occupational Medicine, Hillerød Hospital, Helsevej 2, DK 3400 Hillerød, Denmark (e-mail: bone@noh.regionh.dk).

accepted for publication April 21, 2008.

This review is based on a literature search made in January 2007 on request by the Danish National Board of Industrial Injuries. The search in PubMed, EMBASE, and PsycINFO resulted in more than 1,000 publications. This was reduced to 14 after the titles, abstracts, and papers were evaluated by using the following criteria: 1) a longitudinal study, 2) exposure to work-related psychosocial factors, 3) the outcome a measure of depression, 4) relevant statistical estimates, and 5) nonduplicated publication. Of the 14 studies, seven used standardized diagnostic instruments as measures of depression, whereas the other seven studies used self-administered questionnaires. The authors found moderate evidence for a relation between the psychological demands of the job and the development of depression, with relative risks of approximately 2.0. However, indication of publication bias weakens the evidence. Social support at work was associated with a decrease in risk for future depression, as all four studies dealing with this exposure showed associations with relative risks of about 0.6. Even if this literature study has identified work-related psychosocial factors that in high-quality epidemiologic studies predict depression, studies are still needed that assess in more detail the duration and intensity of exposure necessary for developing depression.

Bone Tox (not Botox) and Cadmium.

BrooklynDodger(s) comment: We think little about cadmium beyond the kidney and respiratory cancer. But "itai-itai" disease is an almost obligatory question on a tox survey exam. The osteoblast osteoclast dialogue explored here reminds us the body process in normal conditions arise from pushes and pulls.


Environmental Toxicology and Pharmacology
Volume 28, Issue 2, September 2009, Pages 232-236

Effects of cadmium on osteoblasts and osteoclasts in vitro

References and further reading may be available for this article. To view references and further reading you must purchase this article.

Xiao Chen^a, Guoying Zhu^{a, ,} , Shuzhu Gu^a, Taiyi Jin^b and Chunlin Shao^c

^aDepartment of Bone Metabolism, Institute of Radiation Medicine, Fudan University, Shanghai 200032, China

^bDepartment of Occupation Medicine, School of Public Health, Fudan University, Shanghai, China

^cDepartment of Radiobiology, Institute of Radiation Medicine, Fudan University, Shanghai, China

Received 19 November 2008;

revised 9 April 2009;

accepted 15 April 2009.

Available online 24 April 2009.

Abstract

Cadmium (Cd) may have direct effects on bone metabolism and the mechanism is not fully understood. To investigate the effects of Cd on bone metabolism, effects of Cd on osteoblasts and osteoclasts in vitro were observed at cellular and molecular levels. Osteoblasts were cultured by sequential enzyme digestion from Sprague–Dawley rats calvarial bone and osteoclasts were isolated from long bones of new-born male and female Sprague–Dawley rats, and then cells were exposed to different concentrations of Cd (0–2.0 μmol/L for osteoblasts; 0.03 μmol/L for osteoclasts). As for osteoblasts, cell viability, alkaline phosphatase (ALP) activity, and mineralization were determined. Osteoprotegerin (OPG) and receptor activator of NF-kB ligand (RANKL) were studied via reverse transcription-polymerase chain reaction (RT-PCR). For osteoclasts, after exposure to Cd (0.03 μmol/L) for 72 h and 120 h, number of osteoclasts and pits formation was observed. Cd inhibited the viability, ALP activity, mineralization and up-regulated RANKL mRNA expression in osteoblasts. But Cd had no obvious effect on OPG mRNA expression. For osteoclasts, cadmium (0.03 μmol/L) could increase the numbers of osteoclasts (p <>p <>

Protein Allergenicity

BrooklynDodger(s) comment: A whole issue of the journal of "don't worry, be happy" on proteins. This is all about GMO's. First, a general toxicology point: ingested proteins do get into the body to do what they do. But in much lower amounts than proteins administered in other ways. Some method of transport through intact membranes. Second, knowing this stuff gets it, it's not loony to be concerned that a proteinaceous pesticide in your corn on the cob might penetrate the body.



* Regulatory Toxicology and Pharmacology
Volume 54, Issue 3, Supplement 1, Pages S1-S62 (August 2009)
Current and future methods for evaluating the allergenic potential of proteins: International workshop, october 23–25, 2007 - ILSI Workshop Oct 07
Edited by Michelle Embry and James E. Gibson
http://www.sciencedirect.com/science/issue/6999-2009-999459996.8998-1320083

Population Levels of Chemicals of Concern

http://www.cdc.gov/exposurereport/pdf/thirdreport_summary.pdf

BrooklynDodger(s) comment: On the ATSDR website is valuable information about population levels of various chemicals of concern - dioxins, pcbs, phthalates, toxic metals, pesticides, PAC metabolites. Present levels may pose a risk - the population rate of diseases includes those caused by these agents - but the risk could only be discovered in humans if there were populations with materially higher exposures than those found in the reference population.

Cobalt Nanoparticles

BrooklynDodger(s) comment: Once again, hazard identification without a measure of potency. Each time a new effect is discovered - in this case migration of particles into the cell - it justifies taking previously identified materials through the same assay. Problem is, every lab has it's own pet assay.


Toxicology Letters
Volume 189, Issue 3, 28 September 2009, Pages 253-259

Engineered cobalt oxide nanoparticles readily enter cells

Elena Papisa, Federica Rossia, Mario Raspantib, Isabella Dalle-Donnec, Graziano Colomboc, Aldo Milzanic, Giovanni Bernardinia, d and Rosalba Gornatia, Corresponding Author Contact Information, E-mail The Corresponding Author

aDepartment of Biotechnology and Molecular Science, Insubria University, Varese, Italy

bDepartment of Human Morphology, Insubria University, Varese, Italy

cDepartment of Biology, University of Milan, Milano, Italy

dCentro di Ricerca Interuniversitario Politecnico di Milano e Università dell’Insubria “The Protein Factory”, Italy

Abstract

Magnetic nanoparticles (NPs) have great potential for applications not only as catalysts or energy storage devices, but also in biomedicine, as contrast enhancement agents for magnetic resonance imaging, or for drug delivery. The same characteristics that make cobalt-based NPs so attractive raise serious questions about their safety. In this context, we investigated Co3O4-NPs. Believing that the characterization of NPs is relevant for understanding their biological activity, we analyzed them by atomic force and electron microscopy to define size, shape, and aggregation. To clarify whether their biological effects could be due to a potential release of cobalt ions, we evaluated spontaneous dissolution in different media. To determine their potential toxicity to human cells, we measured cell viability and ROS formation in two human cell lines using CoCl2 for comparison. Co3O4-NPs induced a concentration- and time-dependent impairment of cellular viability, although cobalt ions were more toxic. We also demonstrated that cobalt causes a rapid induction of ROS if supplied in the form of Co3O4-NPs rather than as ions. Moreover, we evaluated the cellular uptake of NPs. Interestingly, Co3O4-NPs are able to enter the cell very rapidly, remaining confined in vesicles inside the cytoplasm. They were found also inside the cell nuclei, though less frequently.

Tire Dust - Another Urban Air Particulate

Toxicology Letters
Volume 189, Issue 3, 28 September 2009, Pages 206-214

Lung toxicity induced by intratracheal instillation of size-fractionated tire particles

References and further reading may be available for this article. To view references and further reading you must purchase this article.

Paride Mantecca^a, Giulio Sancini^b, Elisa Moschini^a, Francesca Farina^b, Maurizio Gualtieri^a, Annette Rohr^c, Giuseppe Miserocchi^b, Paola Palestini^b and Marina Camatini^{a, ,}

^aDepartment of Environmental Sciences, POLARIS Research Center, University of Milano-Bicocca, 1 piazza della Scienza, Milan 20126, Italy

^bDepartment of Experimental Medicine, POLARIS Research Center, University of Milano-Bicocca, 48 via Cadore, Monza 20052, Italy

^cAir Quality and Health, Electric Power Research Institute (EPRI), 3420 Hillview Avenue, Palo Alto, CA 94304, USA

Abstract

Tire particles (TP) represent a significant component of urban air pollution (PM), constituting more than 10% of PM10 mass at urban locations with heavy traffic. The purpose of this study was to evaluate the effects of size-fractionated TP in an animal exposure model frequently used to assess the health effects of air pollutants. Potential pro-inflammatory and toxic effects of TP2.5 (<2.5 style="font-weight: bold; color: rgb(153, 0, 0);">Inflammatory cellular profiles showed dose-dependent responses after TP10 exposure, while strong cytotoxic effects, including increases in total protein, LDH and AP, were observed to be associated to TP2.5 exposure. Histologically, TP10-treated lungs mainly showed inflammatory tissue infiltration, in contrast to TP2.5-treated lungs, where lysis of the alveolar barrier appeared to be the most characteristic lesion. Our biochemical, cytological, and histological results indicated differential lung toxicity mechanisms elicited by size-fractionated, in agreement with other studies performed in in vivo systems that have shown that lung responses to inhaled or instilled particles are affected by particle size. We conclude that lung toxicity induced by TP10 was primarily due to macrophage-mediated inflammatory events, while toxicity induced by TP2.5 appeared to be related more closely to cytotoxicity.

Dotting the Quantum I's - Engineered nanoparticle toxicity

BrooklynDodger(s): Quantum Dots are engineered nanoparticles, which might be really commentexotic compared to the run of the mill carcinogenic nano particles like diesel particulate matter, carbon black and titanium dioxide. Too bad this investigation didn't explore relative potency between QD's - unlikely to ever undergo an inhalation bioassay, much less present a study in people - with the already known species.


Toxicology and Applied Pharmacology
Volume 238, Issue 2, 15 July 2009, Pages 160-169

Nanoparticles up-regulate tumor necrosis factor-α and CXCL8 via reactive oxygen species and mitogen-activated protein kinase activation

References and further reading may be available for this article. To view references and further reading you must purchase this article.

Hye-Mi Lee^{a, b}, Dong-Min Shin^{a, b}, Hwan-Moon Song^c, Jae-Min Yuk^{a, b}, Zee-Won Lee^d, Sang-Hee Lee^e, Song Mei Hwang^f, Jin-Man Kim^f, Chang-Soo Lee^{c, ,} and Eun-Kyeong Jo^{a, b, g, ,}

^aDepartment of Microbiology, College of Medicine, Daejeon 301-747, South Korea

^bInfection Signaling Network Research Center, College of Medicine, Daejeon 301-747, South Korea

^cDepartment of Chemical Engineering, College of Engineering, Chungnam National University, Daejeon 305-764, South Korea

^dGlycomics Team, Korea Basic Science Institute, Daejeon 305-333, South Korea

^eMolecular Genomics Laboratory, Department of Biological Science, KAIST, 335 Gwahangno, Yuseong-gu, Daejeon 305-701, South Korea

^fDepartment of Pathology, College of Medicine, Daejeon 301-747, South Korea

^gResearch Institute for Medical Sciences, College of Medicine, Daejeon 301-747, South Korea

Abstract

Evaluating the toxicity of nanoparticles is an integral aspect of basic and applied sciences, because imaging applications using traditional organic fluorophores are limited by properties such as photobleaching, spectral overlaps, and operational difficulties. This study investigated the toxicity of nanoparticles and their biological mechanisms. We found that nanoparticles, quantum dots (QDs), considerably activated the production of tumor necrosis factor (TNF)-α and CXC-chemokine ligand (CXCL) 8 through reactive oxygen species (ROS)- and mitogen-activated protein kinases (MAPKs)-dependent mechanisms in human primary monocytes. Nanoparticles elicited a robust activation of intracellular ROS, phosphorylation of p47phox, and nicotinamide adenine dinucleotide phosphate oxidase activities. Blockade of ROS generation with antioxidants significantly abrogated the QD-mediated TNF-α and CXCL8 expression in monocytes. The induced ROS generation subsequently led to the activation of MAPKs, which were crucial for mRNA and protein expression of TNF-α and CXCL8. Furthermore, confocal and electron microscopy analyses showed that internalized QDs were trapped in cytoplasmic vesicles and compartmentalized inside lysosomes. Finally, several repeated intravenous injections of QDs caused an increase in neutrophil infiltration in the lung tissues in vivo. These results provide novel insights into the QD-mediated chemokine induction and inflammatory toxic responses in vitro and in vivo.

Ozone Hole

Toxicology and Applied Pharmacology Volume 236, Issue 3, 1 May 2009, Pages 270-275

Longitudinal distribution of ozone absorption in the lung: Comparison of cigarette smokers and nonsmokers

Melissa L. Bates^{a, ,} , Timothy M. Brenza^b, Abdellaziz Ben-Jebria^{a, b}, Rebecca Bascom^c and James S. Ultman^{a, b}

^aInterdisciplinary Graduate Degree Program in Physiology, Pennsylvania State University, University Park, PA 16802, USA

^bDepartment of Chemical Engineering, Pennsylvania State University, University Park, PA 16802, USA

^cDivision of Pulmonary, Allergy and Critical Care Medicine, Penn State College of Medicine, Hershey, PA 17033, USA

Abstract

In nonsmokers, ozone (O₃) is removed primarily by the epithelial lining fluid (ELF) of the conducting airways. We hypothesized that cigarette smokers, whose ELF antioxidant capacity may be limited by smoking, would remove less O₃ from their conducting airways than nonsmokers. We recruited 29 nonsmokers (17M, 12F) and 30 smokers (19M, 11F, 4 ± 4 pack-years) with similar anthropometric characteristics and measured the longitudinal distribution of O₃ using the bolus inhalation method. We also assessed the physiological effect of this transient exposure regimen using forced spirometry and capnography. Contrary to our hypothesis, the penetration volume at which 50% of a bolus was absorbed was not different between smokers and nonsmokers (97.1 ± 5.4 mL versus 97.9 ± 5.8 mL, p = 0.92). However, smokers did experience an increase in the slope of the alveolar plateau of the capnogram (S_N) (8.1 ± 3.2%, p = 0.02) and a small decrease in FEV₁ (− 1.3 ± 0.6%, p = 0.03), whereas nonsmokers did not (ΔFEV₁ − 0.1 ± 0.5% and ΔS_N − 0.2 ± 2.5%, p > 0.10). Thus, smokers are more sensitive to inhaled O₃ boluses than nonsmokers, despite a similar internal dose distribution.

Cadmium Poses Hazard at Current Population Body Burden Levels

Toxicology and Applied Pharmacology
Volume 238, Issue 3, 1 August 2009, Pages 201-208

Current status of cadmium as an environmental health problem

References and further reading may be available for this article. To view references and further reading you must purchase this article.

Lars Järup^{a, b, ,} and Agneta Åkesson^b

^aDepartment of Epidemiology and Public Health, Imperial College London, UK

^bInstitute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden

Abstract

Cadmium is a toxic metal occurring in the environment naturally and as a pollutant emanating from industrial and agricultural sources. Food is the main source of cadmium intake in the non-smoking population. The bioavailability, retention and toxicity are affected by several factors including nutritional status such as low iron status. Cadmium is efficiently retained in the kidney (half-time 10–30 years) and the concentration is proportional to that in urine (U-Cd). Cadmium is nephrotoxic, initially causing kidney tubular damage. Cadmium can also cause bone damage, either via a direct effect on bone tissue or indirectly as a result of renal dysfunction. After prolonged and/or high exposure the tubular injury may progress to glomerular damage with decreased glomerular filtration rate, and eventually to renal failure. Furthermore, recent data also suggest increased cancer risks and increased mortality in environmentally exposed populations. Dose–response assessment using a variety of early markers of kidney damage has identified U-Cd points of departure for early kidney effects between 0.5 and 3 μg Cd/g creatinine, similar to the points of departure for effects on bone. It can be anticipated that a considerable proportion of the non-smoking adult population has urinary cadmium concentrations of 0.5 μg/g creatinine or higher in non-exposed areas. For smokers this proportion is considerably higher. This implies no margin of safety between the point of departure and the exposure levels in the general population. Therefore, measures should be put in place to reduce exposure to a minimum, and the tolerably daily intake should be set in accordance with recent findings

Evidence for toxicity of carbon based nanoparticles

Toxicology Letters Volume 186, Issue 3, 8 May 2009, Pages 166-173

Genotoxicity of nanomaterials: DNA damage and micronuclei induced by carbon nanotubes and graphite nanofibres in human bronchial epithelial cells in vitro
Hanna K. Lindberga, Ghita C.-M. Falcka, Satu Suhonena, Minnamari Vippolab, c, Esa Vanhalab, Julia Catalána, d, Kai Savolainena and Hannu Norppaa, ,
aNew Technologies and Risks, Work Environment Development, Finnish Institute of Occupational Health, FI-00250 Helsinki, Finland
bAerosols, Dusts and Metals, Work Environment Development, Finnish Institute of Occupational Health, FI-00250 Helsinki, Finland
cDepartment of Materials Science, Tampere University of Technology, FI-33101 Tampere, Finland
dDepartment of Anatomy, Embryology and Genetics, University of Zaragoza, Zaragoza, Spain


Abstract
Despite the increasing industrial use of different nanomaterials, data on their genotoxicity are scant. In the present study, we examined the potential genotoxic effects of carbon nanotubes (CNTs; >50% single-walled, 40% other CNTs; 1.1 nm × 0.5–100 μm; Sigma–Aldrich) and graphite nanofibres (GNFs; 95%; outer diameter 80–200 nm, inner diameter 30–50 nm, length 5–20 μm; Sigma–Aldrich) in vitro. Genotoxicity was assessed by the single cell gel electrophoresis (comet) assay and the micronucleus assay (cytokinesis-block method) in human bronchial epithelial BEAS 2B cells cultured for 24 h, 48 h, or 72 h with various doses (1–100 μg/cm2, corresponding to 3.8–380 μg/ml) of the carbon nanomaterials. In the comet assay, CNTs induced a dose-dependent increase in DNA damage at all treatment times, with a statistically significant effect starting at the lowest dose tested. GNFs increased DNA damage at all doses in the 24-h treatment, at two doses (40 and 100 μg/cm2) in the 48-h treatment (dose-dependent effect) and at four doses (lowest 10 μg/cm2) in the 72-h treatment. In the micronucleus assay, no increase in micronucleated cells was observed with either of the nanomaterials after the 24-h treatment or with CNTs after the 72-h treatment. The 48-h treatment caused a significant increase in micronucleated cells at three doses (lowest 10 μg/cm2) of CNTs and at two doses (5 and 10 μg/cm2) of GNFs. The 72-h treatment with GNFs increased micronucleated cells at four doses (lowest 10 μg/cm2). No dose-dependent effects were seen in the micronucleus assay. The presence of carbon nanomaterial on the microscopic slides disturbed the micronucleus analysis and made it impossible at levels higher than 20 μg/cm2 of GNFs in the 24-h and 48-h treatments. In conclusion, our results suggest that both CNTs and GNFs are genotoxic in human bronchial epithelial BEAS 2B cells in vitro. This activity may be due to the fibrous nature of these carbon nanomaterials with a possible contribution by catalyst metals present in the materials—Co and Mo in CNTs (<5>

Transplacental Carcinogenesis by Arsenic

Toxicology and Applied Pharmacology
Volume 186, Issue 1, 1 January 2003, Pages 7-17

Transplacental carcinogenicity of inorganic arsenic in the drinking water: induction of hepatic, ovarian, pulmonary, and adrenal tumors in mice

References and further reading may be available for this article. To view references and further reading you must purchase this article.

Michael P. Waalkes^{, , a}, Jerrold M. Ward^b, Jie Liu^a and Bhalchandra A. Diwan^c

^a Inorganic Carcinogenesis Section, Laboratory of Comparative Carcinogenesis, National Cancer Institute at the National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA

^b Veterinary and Tumor Pathology Section, Office of Laboratory Animal Science, National Cancer Institute-Frederick, Frederick, MD 21702, USA

^c Intramural Research Support Program, Science Applications International Corp.-Frederick, National Cancer Institute at Frederick, Frederick, MD 21702, USA

Received 14 August 2002;

accepted 10 October 2002. ;

Available online 6 February 2003.

Abstract

Arsenic is a known human carcinogen, but development of rodent models of inorganic arsenic carcinogenesis has been problematic. Since gestation is often a period of high sensitivity to chemical carcinogenesis, we performed a transplacental carcinogenicity study in mice using inorganic arsenic. Groups (n = 10) of pregnant C3H mice were given drinking water containing sodium arsenite (NaAsO₂) at 0 (control), 42.5, and 85 ppm arsenite ad libitum from day 8 to 18 of gestation. These doses were well tolerated and body weights of the dams during gestation and of the offspring subsequent to birth were not reduced. Dams were allowed to give birth, and offspring were weaned at 4 weeks and then put into separate gender-based groups (n = 25) according to maternal exposure level. The offspring received no additional arsenic treatment. The study lasted 74 weeks in males and 90 weeks in females. A complete necropsy was performed on all mice and tissues were examined by light microscopy in a blind fashion. In male offspring, there was a marked increase in hepatocellular carcinoma incidence in a dose- related fashion (control, 12%; 42.5 ppm, 38%; 85 ppm, 61%) and in liver tumor multiplicity (tumors per liver; 5.6-fold over control at 85 ppm). In males, there was also a dose-related increase in adrenal tumor incidence and multiplicity. In female offspring, dose-related increases occurred in ovarian tumor incidence (control, 8%; 42.5 ppm, 26%; 85 ppm, 38%) and lung carcinoma incidence (control, 0%; 42.5 ppm, 4%; 85 ppm, 21%). Arsenic exposure also increased the incidence of proliferative lesions of the uterus and oviduct. These results demonstrate that oral inorganic arsenic exposure, as a single agent, can induce tumor formation in rodents and establishes inorganic arsenic as a complete transplacental carcinogen in mice. The development of this rodent model of inorganic arsenic carcinogenesis has important implications in defining the mechanism of action for this common environmental carcinogen.

Reflections on History of Particulate Air Quality Standards

BrooklynDodger(s) comment: This seems an important review of the evolution of scientific knowledge and public health intervention. Dockery and his work were in the center of the dispute. The Dodger(s) reading of the history is that the epidemiologic evidence emerged in the published literature around 1995 and later, and that toxicologic evidence emerged within the time frame that the new NAAQS limit for PM2.5 was proposed. The NAAQS limits for PM2.5 then proposed of 15 ug/m^3 annual and 65 ug 24-hour were not fully protective and were roughly equivalent to the old PM10 limits. The 2006 NAAQS of 35 ug for 24 hours was the first true reduction in allowable exposure.


Annals of Epidemiology, Volume 19, Issue 4, Pages 257-263
Health Effects of Particulate Air Pollution

Douglas W. Dockery ScD, a,
aDepartments of Environmental Health and Epidemiology, Harvard School of Public Health, Boston, MA

In the 1980's it was generally felt that particulate air pollution concentrations in the United States were not a hazard to the public health. However, in the early 1990's the application of econometric time-series studies and prospective cohort studies suggested increased mortality associated with acute (daily) and chronic (decades) exposures to particulate air pollution commonly observed in the developed world. The epidemiologic evidence was not supported by evidence of causal associations from other disciplines. Nevertheless, the EPA moved to tighten controls on fine particulate air pollution. The debate over the science was played out in public hearings and the courts. The experience provides lessons on the use of epidemiologic data in setting public policy.

Air Pollution Components Activate Inflammatory Genes

BrooklynDodger(s) comment: This raises a concern that complexity could be used in future to obfuscate regulation. Would be good to have some notion of relative potency, although some of these are granular and some have some solubility. It's a bit of a surprise that ZnCl2 is up there with LPS. Hard to think of what could be used as a negative control.


ToxicologyVolume 259, Issues 1-2, 2 May 2009, Pages 46-53

Cytokine and chemokine expression patterns in lung epithelial cells exposed to components characteristic of particulate air pollution


J. Øvrevik, a, , M. Låga, J.A. Holmea, P.E. Schwarzea and M. Refsnesa
aDepartment of Air Pollution and Noise, Division of Environmental Medicine, Norwegian

Abstract
Airborne particulate matter (PM) has a complex composition, and the relative contribution of different compounds to PM-induced effects is only partly understood. The present study compared the capability of selected components commonly found in PM, to induce pro-inflammatory responses in lung epithelial cells. Ultrafine carbon black (ufCB), ZnCl2, FeSO4, 1-nitropyrene (1-NP), lipopolysaccharide (LPS), and crystalline silica (positive control) were screened for effects on the expression of 84 inflammation-related genes in the bronchial epithelial cell line, BEAS-2B. A total of 22 genes were up-regulated by one or more of the tested compounds, and 5 cytokine and 11 chemokine genes were selected for further studies. After 10 h exposure, silica induced significantly increased expression of CCL20, CXCL1/-3/-8/-10/-11, lymphotoxin (LT)β and interleukin (IL)-6; ufCB induced CXCL8/-10 and -11; ZnCl2 induced CCL11/-20/-26, CXCL1/-5/-8/-14 and tumor necrosis factor (TNF)-α; FeSO4 induced a weak up-regulation of CXCL8 and TNF-α; LPS induced CCL20, CXCL1/-5/-8/-10/-11, LTβ and IL-6; and 1-NP induced expression of CCL20, CXCL1/-3/-8, TNF-α and IL-6. Despite obvious differences, all compounds induced response-patterns that correlated relatively well with that of silica, the positive control. The predominant response appeared to be increased gene expression of neutrophil-recruiting CXC-chemokines. CXCL8 was the only gene induced by all tested PM-components, the most up-regulated on average, and also dominating the gene-expression patterns induced by coarse PM. The data show quantitative, and to a certain extent qualitative differences in cytokine/chemokine gene-expression profiles of the compounds tested. However, there were also striking similarities in the response-patterns induced by these physically/chemically widely different compounds.
Keywords: Air pollution; Lung; Epithelium; Inflammation; Cytokines; Gene expression