Saturday, March 21, 2009
Retroactively on Hiatus 2009-3-21 to 2009-4-3
BrooklynDodger(s) comment: The Dodger(s) got distracted by other activities. Hopefully back to the daily grind.
Friday, March 20, 2009
Still Carcinogenic After All These Years
http://monographs.iarc.fr/ENG/Monographs/vol97/index.php
IARC Monographs on the Evaluation of Carcinogenic Risks to Humans
Volume 97 (2008)
1,3-Butadiene, Ethylene Oxide and Vinyl Halides (Vinyl Fluoride, Vinyl Chloride and Vinyl Bromide)
View full volume (510 pages, 6 Mb)
>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
Brooklyn Dodger(s) comment: IARC monographs are now available in full text, working forward from volume 97 and backward from volume 63. Volume 62 - wood dust and formaldehyde, both known to be carcinogenic to humans is next going backward. VF and VB are classified as probably carcinogenic - the others known. The Dodger(s) will discuss the ethylene halides as a group in a future post.
IARC Monographs on the Evaluation of Carcinogenic Risks to Humans
Volume 97 (2008)
1,3-Butadiene, Ethylene Oxide and Vinyl Halides (Vinyl Fluoride, Vinyl Chloride and Vinyl Bromide)
View full volume (510 pages, 6 Mb)
>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
Brooklyn Dodger(s) comment: IARC monographs are now available in full text, working forward from volume 97 and backward from volume 63. Volume 62 - wood dust and formaldehyde, both known to be carcinogenic to humans is next going backward. VF and VB are classified as probably carcinogenic - the others known. The Dodger(s) will discuss the ethylene halides as a group in a future post.
Thursday, March 19, 2009
Arsenic Mechanisms Probed
Detection of trivalent arsenic [As(III)] complex with DNA: A spectroscopic investigation
Authors: S. M. Mandal ab; A. K. Ghosh a; B. R. Pati b; A. K. Das a
Affiliations:
a Department of Biotechnology, Indian Institute of Technology, West Bengal, India
b Department of Microbiology, Vidyasagar University, West Bengal, India
Toxicological & Environmental Chemistry, Volume 91, Issue 2 March 2009 , pages 219 - 224
Abstract
Arsenite [As(III)] is well known to exert mutagenic or carcinogenic effects. Arsenic (III) binds proteins with its cystine-SH group to DNA. Overall binding constant K = 1.12 104 M-1 and exponential decay constant T1 = 271 s for DNA-As (III) interaction were measured spectrophometrically at λmax = 260 nm. Fourier transform infrared (FTIR) spectrometric method was used to charac-terize and determine the arsenite binding site in DNA-As(III) interaction. FTIR spectroscopic results showed that As(III) indirectly binds to the nitrogen bases of DNA and predominantly affected the H-bonded OH and NH bands, whereas no interaction was found with phosphate groups. No transitions from B to A or B to Z was observed in B-DNA structure.
>>>>>>>>>>>>>>>>>
BrooklynDodger(s) (Comment)s: Toxicology and Environmental Chemistry published papers from and with a developing world focus (if India is still the developing world.) Aresenic in ground water for drinking is clearly a bigger issue in Asia than the US and Europe. The Dodger(s) has(had) wondered whether arsenic toxicity arose from arsenic substituting for phosphorous, being just below in the periodic table, sort of like lead substituting for calcium. This paper suggests it's arsenate reacting with DNA rather than arsenic inserting itself.
Authors: S. M. Mandal ab; A. K. Ghosh a; B. R. Pati b; A. K. Das a
Affiliations:
a Department of Biotechnology, Indian Institute of Technology, West Bengal, India
b Department of Microbiology, Vidyasagar University, West Bengal, India
Toxicological & Environmental Chemistry, Volume 91, Issue 2 March 2009 , pages 219 - 224
Abstract
Arsenite [As(III)] is well known to exert mutagenic or carcinogenic effects. Arsenic (III) binds proteins with its cystine-SH group to DNA. Overall binding constant K = 1.12 104 M-1 and exponential decay constant T1 = 271 s for DNA-As (III) interaction were measured spectrophometrically at λmax = 260 nm. Fourier transform infrared (FTIR) spectrometric method was used to charac-terize and determine the arsenite binding site in DNA-As(III) interaction. FTIR spectroscopic results showed that As(III) indirectly binds to the nitrogen bases of DNA and predominantly affected the H-bonded OH and NH bands, whereas no interaction was found with phosphate groups. No transitions from B to A or B to Z was observed in B-DNA structure.
>>>>>>>>>>>>>>>>>
BrooklynDodger(s) (Comment)s: Toxicology and Environmental Chemistry published papers from and with a developing world focus (if India is still the developing world.) Aresenic in ground water for drinking is clearly a bigger issue in Asia than the US and Europe. The Dodger(s) has(had) wondered whether arsenic toxicity arose from arsenic substituting for phosphorous, being just below in the periodic table, sort of like lead substituting for calcium. This paper suggests it's arsenate reacting with DNA rather than arsenic inserting itself.
Wednesday, March 18, 2009
Falling Down Stairs
Applied ErgonomicsVolume 40, Issue 3, May 2009, Pages 348-352
Prevention of falls during stairway descent in older adults
B.J. Kim, a,
aDepartment of Engineering, East Carolina University, Greenville, 229 Slay Hall, Greenville, NC 27858, NC, USA
A prospective design was applied to examine how older adults would adapt stairway intervention stimuli to gait patterns during stairway descent to prevent falls. Ambient lighting and an auditory signal were used as stairway intervention stimuli. The gait pattern changes with and without stimuli were compared. No significant change of angular displacement was found between normal condition and intervention conditions under daylight and nightlight. The lighting intervention tended to increase the knee's angular velocity for both daylight and nightlight conditions, but not the ankle's angular velocity. However, adding the auditory signal to the lighting intervention under nightlight condition increased the ankle's angular velocity. Under the daylight condition, every intervention was significantly helpful to make people step on the floor more confidently compared to the condition without interventions. However, the intervention of lighting had an opposite effect on the confidence of stepping under the nightlight condition. The intervention of lighting may contribute to increase of confidence during stair descent while compromising the declined stride length in older adults and the potential “rush” factor for falls on stairs.
>>>>>>>>>>>>>>>
BrooklynDodger(s) comment: As we get older, falling down stairs is more of risk. Mostly this report demonstrates how it's hard to figure out the risk factors and interventions.
Prevention of falls during stairway descent in older adults
B.J. Kim, a,
aDepartment of Engineering, East Carolina University, Greenville, 229 Slay Hall, Greenville, NC 27858, NC, USA
A prospective design was applied to examine how older adults would adapt stairway intervention stimuli to gait patterns during stairway descent to prevent falls. Ambient lighting and an auditory signal were used as stairway intervention stimuli. The gait pattern changes with and without stimuli were compared. No significant change of angular displacement was found between normal condition and intervention conditions under daylight and nightlight. The lighting intervention tended to increase the knee's angular velocity for both daylight and nightlight conditions, but not the ankle's angular velocity. However, adding the auditory signal to the lighting intervention under nightlight condition increased the ankle's angular velocity. Under the daylight condition, every intervention was significantly helpful to make people step on the floor more confidently compared to the condition without interventions. However, the intervention of lighting had an opposite effect on the confidence of stepping under the nightlight condition. The intervention of lighting may contribute to increase of confidence during stair descent while compromising the declined stride length in older adults and the potential “rush” factor for falls on stairs.
>>>>>>>>>>>>>>>
BrooklynDodger(s) comment: As we get older, falling down stairs is more of risk. Mostly this report demonstrates how it's hard to figure out the risk factors and interventions.
Tuesday, March 17, 2009
Shooting Accuracy with Eyes Wide Shut
Applied ErgonomicsVolume 40, Issue 3, May 2009, Pages 500-508
Pistol shooting accuracy as dependent on experience, eyes being opened and available viewing time
Ravindra S. Goonetilleke, a, , Errol R. Hoffmanna and Wing Chung Laua
aHuman Performance Laboratory, Department of Industrial Engineering and Logistics Management, Hong Kong University of Science and Technology, Clear Water Bay, Hong Kong
A study of the shooting accuracy of three groups of pistol shooters is reported. The groups included (i) experienced gas pistol shooters; (ii) persons with experience in video shooting games; and (iii) persons with no shooting experience. The viewing time was varied in the tests. The results showed that experience had a significant effect on the mean and root mean square (RMS) shooting errors at the target. The results also showed that the viewing time does not need to exceed about 2 s for an experienced pistol shooter and about 3 s for a novice shooter to reach the best performance. Two models for the effects of limited viewing time are proposed; both models fit the data well when the viewing time is less than about 2 s. The results indicated that the differences occurring with varying levels of experience are due to postural balance and not due to the aiming or cognitive component of the task.
>>>>>>>>>>>>>>>>>>>>>
BrooklynDodger(s) comment: The abstract did not address eyes shut. The full text is probably worth reading, although eyes shut shooting has a certain risability from the title.
Pistol shooting accuracy as dependent on experience, eyes being opened and available viewing time
Ravindra S. Goonetilleke, a, , Errol R. Hoffmanna and Wing Chung Laua
aHuman Performance Laboratory, Department of Industrial Engineering and Logistics Management, Hong Kong University of Science and Technology, Clear Water Bay, Hong Kong
A study of the shooting accuracy of three groups of pistol shooters is reported. The groups included (i) experienced gas pistol shooters; (ii) persons with experience in video shooting games; and (iii) persons with no shooting experience. The viewing time was varied in the tests. The results showed that experience had a significant effect on the mean and root mean square (RMS) shooting errors at the target. The results also showed that the viewing time does not need to exceed about 2 s for an experienced pistol shooter and about 3 s for a novice shooter to reach the best performance. Two models for the effects of limited viewing time are proposed; both models fit the data well when the viewing time is less than about 2 s. The results indicated that the differences occurring with varying levels of experience are due to postural balance and not due to the aiming or cognitive component of the task.
>>>>>>>>>>>>>>>>>>>>>
BrooklynDodger(s) comment: The abstract did not address eyes shut. The full text is probably worth reading, although eyes shut shooting has a certain risability from the title.
Monday, March 16, 2009
Ultrafine Allergic Inflammation Shows Complex Pattern
The journal of allergy and clinical immunology [0091-6749] Alessandrini yr.2006 vol.117 iss.4 pg.824
Effects of ultrafine carbon particle inhalation on allergic inflammation of the lung
Francesca Alessandrini PhDa, c, , , Holger Schulz MDb, c, Shinji Takenaka DVM, PhDb, c, Bernd Lentner BScb, Erwin Karg MScb, c, Heidrun Behrendt MDa, c and Thilo Jakob MDa, d
aFrom the Division of Environmental Dermatology and Allergy, GSF/TUM, ZAUM Center for Allergy and Environment, Neuherberg and Munich
bInstitute of Inhalation Biology
cFocus-Network: Aerosols and Health, GSF National Research Center for Environment and Health, Neuherberg
dDepartment of Dermatology and Allergy Biederstein, Technical University Munich
.
Background
Epidemiologic studies show that exposure to particulate air pollution is associated with asthma exacerbation. Ultrafine particles (diameter <100>adjuvant activity of inhaled elemental carbon ultrafine particles (EC-UFPs) on allergic airway inflammation.
Methods
The effects of ultrafine particle inhalation on allergic airway inflammation was analyzed in ovalbumin-sensitized mice and nonsensitized controls. Particle exposure (526 μg/m3, 24 hours) was performed 24, 96, or 168 hours before or 24 or 72 hours after ovalbumin aerosol challenge. Allergic inflammation was analyzed at different time points after allergen challenge by means of bronchoalveolar lavage cell count and cytokine/total protein assays, lung histology, and airway hyperresponsiveness.
Results
In sensitized mice, inhalation of ultrafine particles 24 hours before allergen challenge caused a significant increase of bronchoalveolar lavage inflammatory cell infiltrate, protein, IL-4, IL-5, and IL-13 compared with relevant controls. These adjuvant effects were dose- and time-dependent and were still present when particle exposure was performed 4 days before allergen challenge. The adjuvant effect of ultrafine particles was also documented by increased mucus production, peribronchiolar and perivascular inflammation, and enhanced airway hyperresponsiveness. In contrast, particle exposure in sensitized mice after allergen challenge caused only moderate effects, such as a delay of inflammatory infiltrate and a reduction of cytokines in bronchoalveolar lavage fluid.
Conclusion
Exposure to ultrafine carbon particles before allergen challenge exerts strong adjuvant effects on the manifestation of allergic airway inflammation. Allergen-sensitized individuals may therefore be more susceptible to detrimental health effects of ultrafine particles.
>>>>>>>>>>>>>>>>>>>
BrooklynDodger(s) comments: Sorting the multiple approaches to ultrafine particle induced respiratory effects in short exposure, acute effect studies will be a task for supporting a framework on chronic exposure. The real life scenario would be continuing exposure to ultrafines with periodic exposure to allegen challenges. The exposure was the previously considered inert carbon at .5 mg/m3, which is a lot compared to environmental references and zilch compared to occupational
Effects of ultrafine carbon particle inhalation on allergic inflammation of the lung
Francesca Alessandrini PhDa, c, , , Holger Schulz MDb, c, Shinji Takenaka DVM, PhDb, c, Bernd Lentner BScb, Erwin Karg MScb, c, Heidrun Behrendt MDa, c and Thilo Jakob MDa, d
aFrom the Division of Environmental Dermatology and Allergy, GSF/TUM, ZAUM Center for Allergy and Environment, Neuherberg and Munich
bInstitute of Inhalation Biology
cFocus-Network: Aerosols and Health, GSF National Research Center for Environment and Health, Neuherberg
dDepartment of Dermatology and Allergy Biederstein, Technical University Munich
.
Background
Epidemiologic studies show that exposure to particulate air pollution is associated with asthma exacerbation. Ultrafine particles (diameter <100>adjuvant activity of inhaled elemental carbon ultrafine particles (EC-UFPs) on allergic airway inflammation.
Methods
The effects of ultrafine particle inhalation on allergic airway inflammation was analyzed in ovalbumin-sensitized mice and nonsensitized controls. Particle exposure (526 μg/m3, 24 hours) was performed 24, 96, or 168 hours before or 24 or 72 hours after ovalbumin aerosol challenge. Allergic inflammation was analyzed at different time points after allergen challenge by means of bronchoalveolar lavage cell count and cytokine/total protein assays, lung histology, and airway hyperresponsiveness.
Results
In sensitized mice, inhalation of ultrafine particles 24 hours before allergen challenge caused a significant increase of bronchoalveolar lavage inflammatory cell infiltrate, protein, IL-4, IL-5, and IL-13 compared with relevant controls. These adjuvant effects were dose- and time-dependent and were still present when particle exposure was performed 4 days before allergen challenge. The adjuvant effect of ultrafine particles was also documented by increased mucus production, peribronchiolar and perivascular inflammation, and enhanced airway hyperresponsiveness. In contrast, particle exposure in sensitized mice after allergen challenge caused only moderate effects, such as a delay of inflammatory infiltrate and a reduction of cytokines in bronchoalveolar lavage fluid.
Conclusion
Exposure to ultrafine carbon particles before allergen challenge exerts strong adjuvant effects on the manifestation of allergic airway inflammation. Allergen-sensitized individuals may therefore be more susceptible to detrimental health effects of ultrafine particles.
>>>>>>>>>>>>>>>>>>>
BrooklynDodger(s) comments: Sorting the multiple approaches to ultrafine particle induced respiratory effects in short exposure, acute effect studies will be a task for supporting a framework on chronic exposure. The real life scenario would be continuing exposure to ultrafines with periodic exposure to allegen challenges. The exposure was the previously considered inert carbon at .5 mg/m3, which is a lot compared to environmental references and zilch compared to occupational
Sunday, March 15, 2009
Hazard Identification - Arsenic Causing Cardiovascular Disease
Toxicol. Sci. 2009 107: 312-323; doi:10.1093/toxsci/kfn236.
http://toxsci.oxfordjournals.org/cgi/content/abstract/107/2/312?etoc
Arsenic and Cardiovascular Disease
J. Christopher States*,,1, Sanjay Srivastava,, Yu Chen and Aaron Barchowsky¶
* Department of Pharmacology and Toxicology Center for Environmental Genomics and Integrative Biology Institute of Molecular Cardiology, University of Louisville, Louisville, Kentucky 40292 Departments of Environmental Medicine and Medicine, New York University School of Medicine, New York, New York 10016 ¶ Department of Environmental and Occupational Health, University of Pittsburgh, Pittsburgh, Pennsylvania 15219
1 To whom correspondence should be addressed at Department of Pharmacology & Toxicology, University of Louisville, 570 South Preston Street, Suite 221, Lousiville, KY 40202. Fax: (502) 852-2492. E-mail: jcstates@louisville.edu
Abstract
Chronic arsenic exposure is a worldwide health problem. Although arsenic-induced cancer has been widely studied, comparatively little attention has been paid to arsenic-induced vascular disease. Epidemiological studies have shown that chronic arsenic exposure is associated with increased morbidity and mortality from cardiovascular disease. In addition, studies suggest that susceptibility to arsenic-induced vascular disease may be modified by nutritional factors in addition to genetic factors. Recently, animal models for arsenic-induced atherosclerosis and liver sinusoidal endothelial cell dysfunction have been developed. Initial studies in these models show that arsenic exposure accelerates and exacerbates atherosclerosis in apolipoprotein E–knockout mice. Microarray studies of liver mRNA and micro-RNA abundance in mice exposed in utero suggest that a permanent state of stress is induced by the arsenic exposure. Furthermore, the livers of the arsenic-exposed mice have activated pathways involved in immune responses suggesting a pro-hyperinflammatory state. Arsenic exposure of mice after weaning shows a clear dose-response in the extent of disease exacerbation. In addition, increased inflammation in arterial wall is evident. In response to arsenic-stimulated oxidative signaling, liver sinusoidal endothelium differentiates into a continuous endothelium that limits nutrient exchange and waste elimination. Data suggest that nicotinamide adenine dinucleotide phosphate oxidase–derived superoxide or its derivatives are essential second messengers in the signaling pathway for arsenic-stimulated vessel remodeling. The recent findings provide future directions for research into the cardiovascular effects of arsenic exposure.
>>>>>>>>>>>>>>>>>>>>>
BrooklynDodger(s) comments: The associations of cardiovascular diseases from environmental and occupational chemical exposures are largely unexplored. This review identifies inflammation as a pathway to atherosclerosis. This is likely hard to study in people, since people have many pathways to athero.
http://toxsci.oxfordjournals.org/cgi/content/abstract/107/2/312?etoc
Arsenic and Cardiovascular Disease
J. Christopher States*,,1, Sanjay Srivastava,, Yu Chen and Aaron Barchowsky¶
* Department of Pharmacology and Toxicology Center for Environmental Genomics and Integrative Biology Institute of Molecular Cardiology, University of Louisville, Louisville, Kentucky 40292 Departments of Environmental Medicine and Medicine, New York University School of Medicine, New York, New York 10016 ¶ Department of Environmental and Occupational Health, University of Pittsburgh, Pittsburgh, Pennsylvania 15219
1 To whom correspondence should be addressed at Department of Pharmacology & Toxicology, University of Louisville, 570 South Preston Street, Suite 221, Lousiville, KY 40202. Fax: (502) 852-2492. E-mail: jcstates@louisville.edu
Abstract
Chronic arsenic exposure is a worldwide health problem. Although arsenic-induced cancer has been widely studied, comparatively little attention has been paid to arsenic-induced vascular disease. Epidemiological studies have shown that chronic arsenic exposure is associated with increased morbidity and mortality from cardiovascular disease. In addition, studies suggest that susceptibility to arsenic-induced vascular disease may be modified by nutritional factors in addition to genetic factors. Recently, animal models for arsenic-induced atherosclerosis and liver sinusoidal endothelial cell dysfunction have been developed. Initial studies in these models show that arsenic exposure accelerates and exacerbates atherosclerosis in apolipoprotein E–knockout mice. Microarray studies of liver mRNA and micro-RNA abundance in mice exposed in utero suggest that a permanent state of stress is induced by the arsenic exposure. Furthermore, the livers of the arsenic-exposed mice have activated pathways involved in immune responses suggesting a pro-hyperinflammatory state. Arsenic exposure of mice after weaning shows a clear dose-response in the extent of disease exacerbation. In addition, increased inflammation in arterial wall is evident. In response to arsenic-stimulated oxidative signaling, liver sinusoidal endothelium differentiates into a continuous endothelium that limits nutrient exchange and waste elimination. Data suggest that nicotinamide adenine dinucleotide phosphate oxidase–derived superoxide or its derivatives are essential second messengers in the signaling pathway for arsenic-stimulated vessel remodeling. The recent findings provide future directions for research into the cardiovascular effects of arsenic exposure.
>>>>>>>>>>>>>>>>>>>>>
BrooklynDodger(s) comments: The associations of cardiovascular diseases from environmental and occupational chemical exposures are largely unexplored. This review identifies inflammation as a pathway to atherosclerosis. This is likely hard to study in people, since people have many pathways to athero.
Saturday, March 14, 2009
MIBK by inhalation - Easy Come, Easy Go
Simulation of repeated dose kinetics of methyl isobutyl ketone in humans from experimental single-dose inhalation exposure
Regulatory Toxicology and Pharmacology, Volume 52, Issue 2, November 2008, Pages 180-188
Shakil A. Saghir, David L. Rick
Abstract
Methyl isobutyl ketone (MIBK) is a solvent used in numerous products and processes and may be present in the air of the workplace as a vapor. The American Conference of Governmental Industrial Hygienists (ACGIH) threshold limit value-time-weighted average (TLV-TWA) and TLV-short term exposure limit (TLV-STEL) for MIBK are 50 and 75 ppm, respectively. These workplace air concentration limits were set to protect workers from irritation, neurasthenic symptoms and possible adverse effects to their livers and kidneys. A recent revision of the ACGIH limit value has been proposed, to reduce the current TLV-TWA to 30 ppm. This article predicts the kinetics and accumulation of MIBK in humans exposed repeatedly in various exposure scenarios (8, 12, and 24 h/day for 7 days) to the current ACGIH TLV-TWA of 50 ppm. The kinetic parameters of the model were derived from published human time-course blood MIBK data from a single 2 h inhalation exposure to 48.9 ppm MIBK. The model correctly simulated single exposure experimental data with a rapid rise in blood concentration to 1.06 μg/ml within 1 h and approached 99% steady-state blood level in 4 h of exposure. MIBK was predicted to be rapidly eliminated from blood after terminating the exposure, reaching 0.53 μg/ml and 0.13 μg/ml within 0.5 and 2 h post-exposure, respectively. Within 4 h after the termination of exposure, blood concentration would be expected to
>>>>>>>>>>
Brooklyn Dodger(s) comments: This is the last of the MIBK trilogy. For this chemical, the TLV and PEL are now the same, a sign of no new data or no material change in perception of toxic potential or potency since 1968. The important finding is that this solvent reaches equilibrium in blood level after 4 hours at 50 ppm.
Regulatory Toxicology and Pharmacology, Volume 52, Issue 2, November 2008, Pages 180-188
Shakil A. Saghir, David L. Rick
Abstract
Methyl isobutyl ketone (MIBK) is a solvent used in numerous products and processes and may be present in the air of the workplace as a vapor. The American Conference of Governmental Industrial Hygienists (ACGIH) threshold limit value-time-weighted average (TLV-TWA) and TLV-short term exposure limit (TLV-STEL) for MIBK are 50 and 75 ppm, respectively. These workplace air concentration limits were set to protect workers from irritation, neurasthenic symptoms and possible adverse effects to their livers and kidneys. A recent revision of the ACGIH limit value has been proposed, to reduce the current TLV-TWA to 30 ppm. This article predicts the kinetics and accumulation of MIBK in humans exposed repeatedly in various exposure scenarios (8, 12, and 24 h/day for 7 days) to the current ACGIH TLV-TWA of 50 ppm. The kinetic parameters of the model were derived from published human time-course blood MIBK data from a single 2 h inhalation exposure to 48.9 ppm MIBK. The model correctly simulated single exposure experimental data with a rapid rise in blood concentration to 1.06 μg/ml within 1 h and approached 99% steady-state blood level in 4 h of exposure. MIBK was predicted to be rapidly eliminated from blood after terminating the exposure, reaching 0.53 μg/ml and 0.13 μg/ml within 0.5 and 2 h post-exposure, respectively. Within 4 h after the termination of exposure, blood concentration would be expected to
>>>>>>>>>>
Brooklyn Dodger(s) comments: This is the last of the MIBK trilogy. For this chemical, the TLV and PEL are now the same, a sign of no new data or no material change in perception of toxic potential or potency since 1968. The important finding is that this solvent reaches equilibrium in blood level after 4 hours at 50 ppm.
Friday, March 13, 2009
Houdini Alert - Formerly "less" toxic ketone causes cancer and kidney damage
ToxicologyVolume 258, Issues 2-3, 28 April 2009, Pages 131-138
Methyl isobutyl ketone (MIBK) induction of α2u-globulin nephropathy in male, but not female rats
.
S.J. Borghoffa, , , G.C. Hardb, N.M. Berdascoc, R. Gingelld, S.M. Greene and W. Gulledgef
aIntegrated Laboratory Systems Inc., Division of Investigative Toxicology, P.O. Box 13501, Research Triangle Park, NC 27709, United States
bPrivate Consultant, Tairua 3508, New Zealand
cDow Chemical Company, Midland, MI 48640, United States
dShell Oil Company, Houston, TX 77210, United States
eThe Eastman Chemical Company, Kingsport, TN 37660, United States
fAmerican Chemistry Council, Arlington, VA 22209, United States
Abstract
Male F-344 rats were administered corn oil (vehicle control), d-limonene (positive control, 300 mg/kg), or MIBK (1000 mg/kg) and female F-344 rats corn oil (vehicle control) or MIBK for 10 consecutive days by oral gavage. Approximately 24 h after the final dose the kidneys were excised and the left kidney prepared and evaluated for histological changes including protein (hyaline) droplet accumulation, immunohistochemical staining for α2u-globulin (α2u), and proliferating cell nuclear antigen (PCNA) to quantitate renal cell proliferation. The right kidney was prepared for quantitation of total protein and α2u using an ELISA. MIBK elicited an increase in protein droplets, accumulation of α2u, and renal cell proliferation in male, but not female rats, responses characteristic of α2u-mediated nephropathy. MIBK produced identical histopathological changes in the male rat kidney when compared to d-limonene, an acknowledged inducer of α2u-nephropathy except that the grade of severity tended to be slightly lower with MIBK. MIBK did not induce any effects in female rats. Therefore, renal histopathology, along with the other measures of α2u accumulation, provides additional weight of evidence to support the inclusion of MIBK in the category of chemicals exerting renal effects through a α2u-nephropathy-mediated mode-of-action.
>>>>>>>>>>>>>>>>>>>
BrooklynDodger(s) comments: The credit line for the lead author reminds us that the Houdini complex has set up shop in the Research Triangle, next door to NIEHS, NTP and EPA NCEA. That's also the site of the facility formerly known as the Chemical Industry Institute for Toxicology. The Houdini attack on hazard determination aims to knock out tumor sites, species and genders one-by-one until there's not enough left for classification. While NTP was running the bioassay of MIBK, Dow, Shell, Eastman and the organization formerly known at the Chemical Manufacturer's Association were at work on making the bioassay disappear.
Alpha-2 (male rat kidney) may be considered the "mother of all Houdini risk assessments," if size and impact is the criterion (gasoline), although it was not the ancestress in the way bladder stones were used against saccharine and melamine. In the bioassay, MIBK caused nephropathy in the female mice. Like gasoline, but unlike limonene, MIBK caused liver tumors in mice of both genders.
However, EPA has chosen to ignore the liver tumors from gasoline, so it can ignore the kidney tumors as well, so as to ignore the need to regulate gasoline as a carcinogen.
Methyl isobutyl ketone (MIBK) induction of α2u-globulin nephropathy in male, but not female rats
.
S.J. Borghoffa, , , G.C. Hardb, N.M. Berdascoc, R. Gingelld, S.M. Greene and W. Gulledgef
aIntegrated Laboratory Systems Inc., Division of Investigative Toxicology, P.O. Box 13501, Research Triangle Park, NC 27709, United States
bPrivate Consultant, Tairua 3508, New Zealand
cDow Chemical Company, Midland, MI 48640, United States
dShell Oil Company, Houston, TX 77210, United States
eThe Eastman Chemical Company, Kingsport, TN 37660, United States
fAmerican Chemistry Council, Arlington, VA 22209, United States
Abstract
Male F-344 rats were administered corn oil (vehicle control), d-limonene (positive control, 300 mg/kg), or MIBK (1000 mg/kg) and female F-344 rats corn oil (vehicle control) or MIBK for 10 consecutive days by oral gavage. Approximately 24 h after the final dose the kidneys were excised and the left kidney prepared and evaluated for histological changes including protein (hyaline) droplet accumulation, immunohistochemical staining for α2u-globulin (α2u), and proliferating cell nuclear antigen (PCNA) to quantitate renal cell proliferation. The right kidney was prepared for quantitation of total protein and α2u using an ELISA. MIBK elicited an increase in protein droplets, accumulation of α2u, and renal cell proliferation in male, but not female rats, responses characteristic of α2u-mediated nephropathy. MIBK produced identical histopathological changes in the male rat kidney when compared to d-limonene, an acknowledged inducer of α2u-nephropathy except that the grade of severity tended to be slightly lower with MIBK. MIBK did not induce any effects in female rats. Therefore, renal histopathology, along with the other measures of α2u accumulation, provides additional weight of evidence to support the inclusion of MIBK in the category of chemicals exerting renal effects through a α2u-nephropathy-mediated mode-of-action.
>>>>>>>>>>>>>>>>>>>
BrooklynDodger(s) comments: The credit line for the lead author reminds us that the Houdini complex has set up shop in the Research Triangle, next door to NIEHS, NTP and EPA NCEA. That's also the site of the facility formerly known as the Chemical Industry Institute for Toxicology. The Houdini attack on hazard determination aims to knock out tumor sites, species and genders one-by-one until there's not enough left for classification. While NTP was running the bioassay of MIBK, Dow, Shell, Eastman and the organization formerly known at the Chemical Manufacturer's Association were at work on making the bioassay disappear.
Alpha-2 (male rat kidney) may be considered the "mother of all Houdini risk assessments," if size and impact is the criterion (gasoline), although it was not the ancestress in the way bladder stones were used against saccharine and melamine. In the bioassay, MIBK caused nephropathy in the female mice. Like gasoline, but unlike limonene, MIBK caused liver tumors in mice of both genders.
However, EPA has chosen to ignore the liver tumors from gasoline, so it can ignore the kidney tumors as well, so as to ignore the need to regulate gasoline as a carcinogen.
Thursday, March 12, 2009
Toxicology of Enriched and Depleted Uranium
ToxicologyVolume 258, Issue 1, 5 April 2009, Pages 1-9
Different pattern of brain pro-/anti-oxidant activity between depleted and enriched uranium in chronically exposed rats
P. Lestaevel, a, , E. Romero1, a, B. Dhieuxa, H. Ben Soussana, H. Berradia, I. Dublineaua, P. Voisina and P. Gourmelona
aInstitut de Radioprotection et de Sûreté Nucléaire, Direction de la RadioProtection de l’Homme, Service de Radiobiologie et d’Epidémiologie, Laboratoire de RadioToxicologie Expérimentale. IRSN, B.P. n°17, F 92262 Fontenay-aux-Roses Cedex, France
Abstract
Uranium is not only a heavy metal but also an alpha particle emitter. The main toxicity of uranium is expected to be due to chemiotoxicity rather than to radiotoxicity. Some studies have demonstrated that uranium induced some neurological disturbances, but without clear explanations. A possible mechanism of this neurotoxicity could be the oxidative stress induced by reactive oxygen species imbalance. The aim of the present study was to determine whether a chronic ingestion of uranium induced anti-oxidative defence mechanisms in the brain of rats. Rats received depleted (DU) or 4% enriched (EU) uranyl nitrate in the drinking water at 2 mg−1 kg−1 day−1 for 9 months. Cerebral cortex analyses were made by measuring mRNA and protein levels and enzymatic activities. Lipid peroxidation, an oxidative stress marker, was significantly enhanced after EU exposure, but not after DU. The gene expression or activity of the main antioxidant enzymes, i.e. superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx), increased significantly after chronic exposure to DU. On the contrary, oral EU administration induced a decrease of these antioxidant enzymes. The NO-ergic pathway was almost not perturbed by DU or EU exposure. Finally, DU exposure increased significantly the transporters (Divalent-Metal-Transporter1; DMT1), the storage molecule (ferritin) and the ferroxidase enzyme (ceruloplasmin), but not EU. These results illustrate that oxidative stress plays a key role in the mechanism of uranium neurotoxicity. They showed that chronic exposure to DU, but not EU, seems to induce an increase of several antioxidant agents in order to counteract the oxidative stress. Finally, these results demonstrate the importance of the double toxicity, chemical and radiological, of uranium.
>>>>>>>>>>>>>>>>>>>
BrooklynDodger(s) Comment: A heavy duty health physicist should address whether the difference in REMS plausibly accounts for the difference in toxicity.
Different pattern of brain pro-/anti-oxidant activity between depleted and enriched uranium in chronically exposed rats
P. Lestaevel, a, , E. Romero1, a, B. Dhieuxa, H. Ben Soussana, H. Berradia, I. Dublineaua, P. Voisina and P. Gourmelona
aInstitut de Radioprotection et de Sûreté Nucléaire, Direction de la RadioProtection de l’Homme, Service de Radiobiologie et d’Epidémiologie, Laboratoire de RadioToxicologie Expérimentale. IRSN, B.P. n°17, F 92262 Fontenay-aux-Roses Cedex, France
Abstract
Uranium is not only a heavy metal but also an alpha particle emitter. The main toxicity of uranium is expected to be due to chemiotoxicity rather than to radiotoxicity. Some studies have demonstrated that uranium induced some neurological disturbances, but without clear explanations. A possible mechanism of this neurotoxicity could be the oxidative stress induced by reactive oxygen species imbalance. The aim of the present study was to determine whether a chronic ingestion of uranium induced anti-oxidative defence mechanisms in the brain of rats. Rats received depleted (DU) or 4% enriched (EU) uranyl nitrate in the drinking water at 2 mg−1 kg−1 day−1 for 9 months. Cerebral cortex analyses were made by measuring mRNA and protein levels and enzymatic activities. Lipid peroxidation, an oxidative stress marker, was significantly enhanced after EU exposure, but not after DU. The gene expression or activity of the main antioxidant enzymes, i.e. superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx), increased significantly after chronic exposure to DU. On the contrary, oral EU administration induced a decrease of these antioxidant enzymes. The NO-ergic pathway was almost not perturbed by DU or EU exposure. Finally, DU exposure increased significantly the transporters (Divalent-Metal-Transporter1; DMT1), the storage molecule (ferritin) and the ferroxidase enzyme (ceruloplasmin), but not EU. These results illustrate that oxidative stress plays a key role in the mechanism of uranium neurotoxicity. They showed that chronic exposure to DU, but not EU, seems to induce an increase of several antioxidant agents in order to counteract the oxidative stress. Finally, these results demonstrate the importance of the double toxicity, chemical and radiological, of uranium.
>>>>>>>>>>>>>>>>>>>
BrooklynDodger(s) Comment: A heavy duty health physicist should address whether the difference in REMS plausibly accounts for the difference in toxicity.
Wednesday, March 11, 2009
Do Cars Cause Cancer?
(Cancer Epidemiol Biomarkers Prev 2009;18(3):760–4)
Lung Adenocarcinoma Incidence Rates and Their Relation to Motor Vehicle Density
Fan Chen, Haley Jackson and William F. Bina
Department of Community Medicine, Mercer University School of Medicine, Macon, Georgia
Requests for reprints: Fan Chen, Department of Community Medicine, Mercer University School of Medicine, 1550 College Street, Macon, GA 31207. Phone: 478-301-4095; Fax: 478-301-2221. E-mail: chen_fd@Mercer.edu
Background and Objective: The temporal trend of adenocarcinoma incidence rates of the lung (ADL) has been reported to parallel the trend of nitrogen oxide (NOx) emissions in the United States. This study explores the geographic pattern of ADL incidence and its relation to motor vehicle density, the major indicator of NOx emissions before 1970.
Methods: ADL incidence rates by counties were retrieved from the nine sites of Surveillance, Epidemiology, and End Results (SEER) Program for the period of 1973 to 1990. Motor vehicle densities by county in 1970 for these SEER sites were estimated according to the numbers of motor vehicle registration and the size of each county. Regression analysis was done with the data of motor vehicle density by counties.
Results: A dose-response pattern between motor vehicle density and ADL incidence was found. The risks are 136% and 68% higher for ADL and squamous cell carcinoma, respectively, for male residents living in areas with 937 motor vehicles per square mile, compared with those living in areas with about one motor vehicle per square mile. The R2 are as high as 0.805 and 0.504 in regressions for male incidence rates of ADL and squamous cell carcinoma, respectively, with the vehicle density values. As a comparison, the prostate cancer incidence rates did not show dose-response relationship with motor vehicle density. If the effect of NOx emissions on ADL incidence rates can be proved by further studies, the current standard of allowance of NOx emissions may need to be revised.
>>>>>>>>>>>>>>>>>>>
BrooklynDodger(s) Comment: Some secondary data analysis, a project done because it can be done. Who knows what confounding lurks beneath the surface. The Dodger(s) would not put his(their) money on NOX, not sure how to distinguish from PM.
Lung Adenocarcinoma Incidence Rates and Their Relation to Motor Vehicle Density
Fan Chen, Haley Jackson and William F. Bina
Department of Community Medicine, Mercer University School of Medicine, Macon, Georgia
Requests for reprints: Fan Chen, Department of Community Medicine, Mercer University School of Medicine, 1550 College Street, Macon, GA 31207. Phone: 478-301-4095; Fax: 478-301-2221. E-mail: chen_fd@Mercer.edu
Background and Objective: The temporal trend of adenocarcinoma incidence rates of the lung (ADL) has been reported to parallel the trend of nitrogen oxide (NOx) emissions in the United States. This study explores the geographic pattern of ADL incidence and its relation to motor vehicle density, the major indicator of NOx emissions before 1970.
Methods: ADL incidence rates by counties were retrieved from the nine sites of Surveillance, Epidemiology, and End Results (SEER) Program for the period of 1973 to 1990. Motor vehicle densities by county in 1970 for these SEER sites were estimated according to the numbers of motor vehicle registration and the size of each county. Regression analysis was done with the data of motor vehicle density by counties.
Results: A dose-response pattern between motor vehicle density and ADL incidence was found. The risks are 136% and 68% higher for ADL and squamous cell carcinoma, respectively, for male residents living in areas with 937 motor vehicles per square mile, compared with those living in areas with about one motor vehicle per square mile. The R2 are as high as 0.805 and 0.504 in regressions for male incidence rates of ADL and squamous cell carcinoma, respectively, with the vehicle density values. As a comparison, the prostate cancer incidence rates did not show dose-response relationship with motor vehicle density. If the effect of NOx emissions on ADL incidence rates can be proved by further studies, the current standard of allowance of NOx emissions may need to be revised.
>>>>>>>>>>>>>>>>>>>
BrooklynDodger(s) Comment: Some secondary data analysis, a project done because it can be done. Who knows what confounding lurks beneath the surface. The Dodger(s) would not put his(their) money on NOX, not sure how to distinguish from PM.
Tuesday, March 10, 2009
Pop Goes the Sociobiologist
The Times op-ed section a while ago published a peculiarly conflicted pop science account of sociobiology. Pinker's account reads like a blog posting someone should have read over or submitted to peer review.
[The original article has been removed to the Times pay site, but it might be found at his Harvard promotion site.] http://pinker.wjh.harvard.edu/articles/
Sniffing Out the Gay Gene
By STEVEN PINKER Published: May 17, 2005 Cambridge, Mass.
A team of Swedish neuroscientists scanned people's brains as they smelled a testosterone derivative found in men's sweat and an estrogen-like compound found in women's urine. In heterosexual men, a part of the hypothalamus (the seat of physical drives) responded to the female compound but not the male one; in heterosexual women and homosexual men, it was the other way around. What is evolutionarily adaptive and what is morally justifiable have little to do with each other. Many laudable activities - being faithful to one's spouse, turning the other cheek, treating every child as precious, loving thy neighbor as thyself - are "biological errors" and are rare or unknown in the natural world.
Steven Pinker, a professor of cognitive science at Harvard, is the author of "How the Mind Works" and "The Blank Slate."
>>>>>>>>>>>>>>>>>>>>>
BrooklynDodger(s) comment: Steven Pinker published a popular book on language and cognition, "The Language Instinct," when on the faculty at MIT. Now it appears he's moved west on Mass Ave to Harvard. Linguistics at MIT was the fort from which Noam Chomsky launched a scientific revolution, and also his personal political campaign to remake thinking about first the Vietnam War, imperialism generally, and the middle east.
The "Language Instinct" was an interesting book, with a lot of computational stuff on language recognition which appeared convincing, perhaps because it was recondite and reflective of computer programming logic.
Since then, Pinker has gone over to the dark side. The paragraphs above are pretty bogus, an example of the arrogance of going beyond a technical range and trading on academic credentials.
First, the Dodger(s) wants to see some inter-rater variability data on these brain MRI's before even crediting the observation in the first place. The Dodger(s) doesn't(don't) doubt that female hormones lit up one of the straight guys, whose brain scan made the publication, and air-balled a gay guy, whose picture also made it.
What's the scoring system, how many were scanned, how were straight and gay determined, all of that stuff.
Second, the sociobiology of evaluating every trait in a phenotype as having to be adaptive is bogus, generating just-so stories. Some stuff is there as a by product of something else which does create a selection advantage.
Third, the second paragraph dumps the entire literature on re-iterated prisoner's dilemma. Cooperation benefits the species, exploitation diminishes the species. The mechanisms by which cooperation is enhanced and preserved are a subject of study. For people, it's not how many children a male can procreate, it's how many of them which prosper and procreate which enhances the penetration of some genetic trait in the male in the population. Men taking care of children rather than running out can be adaptive in the circumstance where nurture is important. Maybe more adaptive now than it was before agriculture was invented 10,00 years ago.
Both types of traits are also carried by females, and may be expressed in females [perhaps in a different way] and impact their reproductive success, and that of offspring. Likewise female traits.
[The original article has been removed to the Times pay site, but it might be found at his Harvard promotion site.] http://pinker.wjh.harvard.edu/articles/
Sniffing Out the Gay Gene
By STEVEN PINKER Published: May 17, 2005 Cambridge, Mass.
A team of Swedish neuroscientists scanned people's brains as they smelled a testosterone derivative found in men's sweat and an estrogen-like compound found in women's urine. In heterosexual men, a part of the hypothalamus (the seat of physical drives) responded to the female compound but not the male one; in heterosexual women and homosexual men, it was the other way around. What is evolutionarily adaptive and what is morally justifiable have little to do with each other. Many laudable activities - being faithful to one's spouse, turning the other cheek, treating every child as precious, loving thy neighbor as thyself - are "biological errors" and are rare or unknown in the natural world.
Steven Pinker, a professor of cognitive science at Harvard, is the author of "How the Mind Works" and "The Blank Slate."
>>>>>>>>>>>>>>>>>>>>>
BrooklynDodger(s) comment: Steven Pinker published a popular book on language and cognition, "The Language Instinct," when on the faculty at MIT. Now it appears he's moved west on Mass Ave to Harvard. Linguistics at MIT was the fort from which Noam Chomsky launched a scientific revolution, and also his personal political campaign to remake thinking about first the Vietnam War, imperialism generally, and the middle east.
The "Language Instinct" was an interesting book, with a lot of computational stuff on language recognition which appeared convincing, perhaps because it was recondite and reflective of computer programming logic.
Since then, Pinker has gone over to the dark side. The paragraphs above are pretty bogus, an example of the arrogance of going beyond a technical range and trading on academic credentials.
First, the Dodger(s) wants to see some inter-rater variability data on these brain MRI's before even crediting the observation in the first place. The Dodger(s) doesn't(don't) doubt that female hormones lit up one of the straight guys, whose brain scan made the publication, and air-balled a gay guy, whose picture also made it.
What's the scoring system, how many were scanned, how were straight and gay determined, all of that stuff.
Second, the sociobiology of evaluating every trait in a phenotype as having to be adaptive is bogus, generating just-so stories. Some stuff is there as a by product of something else which does create a selection advantage.
Third, the second paragraph dumps the entire literature on re-iterated prisoner's dilemma. Cooperation benefits the species, exploitation diminishes the species. The mechanisms by which cooperation is enhanced and preserved are a subject of study. For people, it's not how many children a male can procreate, it's how many of them which prosper and procreate which enhances the penetration of some genetic trait in the male in the population. Men taking care of children rather than running out can be adaptive in the circumstance where nurture is important. Maybe more adaptive now than it was before agriculture was invented 10,00 years ago.
Both types of traits are also carried by females, and may be expressed in females [perhaps in a different way] and impact their reproductive success, and that of offspring. Likewise female traits.
Monday, March 09, 2009
Toxicity and carcinogenicity of methyl isobutyl ketone in F344N rats and B6C3F1 mice following 2-year inhalation exposureToxicology, Volume 244, Issues 2-3, 28 February 2008, Pages 209-219
Matthew D. Stout, Ronald A. Herbert, Grace E. Kissling, Fernando Suarez, Joseph H. Roycroft, Rajendra S. Chhabra, John R. Bucher
Abstract
Methyl isobutyl ketone (MIBK) is primarily used as a denaturant for rubbing alcohol, as a solvent and in the manufacture of methyl amyl alcohol. Inhalation of vapors is the most likely route of exposure in the work place. In order to evaluate the potential of MIBK to induce toxic and carcinogenic effects following chronic exposure, groups of 50 male and 50 female F344/N rats and B6C3F1 mice were exposed to MIBK at concentrations of 0, 450, 900, or 1800 ppm by inhalation, 6 h/day, 5 days per week for 2 years. Survival was decreased in male rats at 1800 ppm. Body weight gains were decreased in male rats at 900 and 1800 ppm and in female mice at 1800 ppm. The primary targets of MIBK toxicity and carcinogenicity were the kidney in rats and the liver in mice. In male rats, there was increased mineralization of the renal papilla at all exposure concentrations. The incidence of chronic progressive nephropathy (CPN) was increased at 1800 ppm and the severity was increased in all exposed groups. There were also increases in renal tubule hyperplasia at all exposure concentrations, and in adenoma and adenoma or carcinoma (combined) at 1800 ppm; these lesions are thought to represent a continuum in the progression of proliferative lesions in renal tubule epithelium. These increases may have resulted from the increased severity of CPN, either through α2μ-globulin-dependent or -independent mechanisms. An increase in mononuclear cell leukemia at 1800 ppm was an uncertain finding. Adrenal medulla hyperplasia was increased at 1800 ppm, and there was a positive trend for increases in benign or malignant pheochromocytomas (combined). In female rats, there were increases in the incidence of CPN in all exposure concentrations and in the severity at 1800 ppm, indicating that CPN was increased by mechanisms in addition to those related to α2μ-globulin. There were renal mesenchymal tumors, which have not been observed in historical control animals, in two female rats at 1800 ppm. The relationship of these tumors to exposure to MIBK was uncertain. Hepatocellular adenomas, and adenoma or carcinoma (combined) were increased in male and female mice exposed to 1800 ppm. There were also treatment-related increases in multiple adenomas in both sexes
>>>>>>>>>>>>>>>>>>
BrooklynDodger(s) comment: This publication of an NTP study left the levels of evidence out of the abstract. These were "Under the conditions of these 2-year studies, there was some evidence of carcinogenic activity of methyl isobutyl ketone in male F344/N rats based on increased incidences of renal tubule neoplasms. Increased incidences of mononuclear cell leukemia in 1,800 ppm male F344/N rats may have been related to methyl isobutyl ketone exposure. There was equivocal evidence of carcinogenic activity of methyl isobutyl ketone in female F344/N rats based on the occurrence of renal mesenchymal tumors in the 1,800 ppm group. There was some evidence of carcinogenic activity of methyl isobutyl ketone in male and female B6C3F1 mice based on increased incidences of liver neoplasms." "Some" evidence is a study finding associations. The nephropathy in female rats undermines the Houdini alpha-2 theory. Liver tumors in both genders of mice is a strong finding. The Dodger(s) would add these findings up to a solid 2B carcinogen at IARC, or reasonably anticipated for the ROC. This is a rare organic vapor that didn't cause lung tumors in mice.
Matthew D. Stout, Ronald A. Herbert, Grace E. Kissling, Fernando Suarez, Joseph H. Roycroft, Rajendra S. Chhabra, John R. Bucher
Abstract
Methyl isobutyl ketone (MIBK) is primarily used as a denaturant for rubbing alcohol, as a solvent and in the manufacture of methyl amyl alcohol. Inhalation of vapors is the most likely route of exposure in the work place. In order to evaluate the potential of MIBK to induce toxic and carcinogenic effects following chronic exposure, groups of 50 male and 50 female F344/N rats and B6C3F1 mice were exposed to MIBK at concentrations of 0, 450, 900, or 1800 ppm by inhalation, 6 h/day, 5 days per week for 2 years. Survival was decreased in male rats at 1800 ppm. Body weight gains were decreased in male rats at 900 and 1800 ppm and in female mice at 1800 ppm. The primary targets of MIBK toxicity and carcinogenicity were the kidney in rats and the liver in mice. In male rats, there was increased mineralization of the renal papilla at all exposure concentrations. The incidence of chronic progressive nephropathy (CPN) was increased at 1800 ppm and the severity was increased in all exposed groups. There were also increases in renal tubule hyperplasia at all exposure concentrations, and in adenoma and adenoma or carcinoma (combined) at 1800 ppm; these lesions are thought to represent a continuum in the progression of proliferative lesions in renal tubule epithelium. These increases may have resulted from the increased severity of CPN, either through α2μ-globulin-dependent or -independent mechanisms. An increase in mononuclear cell leukemia at 1800 ppm was an uncertain finding. Adrenal medulla hyperplasia was increased at 1800 ppm, and there was a positive trend for increases in benign or malignant pheochromocytomas (combined). In female rats, there were increases in the incidence of CPN in all exposure concentrations and in the severity at 1800 ppm, indicating that CPN was increased by mechanisms in addition to those related to α2μ-globulin. There were renal mesenchymal tumors, which have not been observed in historical control animals, in two female rats at 1800 ppm. The relationship of these tumors to exposure to MIBK was uncertain. Hepatocellular adenomas, and adenoma or carcinoma (combined) were increased in male and female mice exposed to 1800 ppm. There were also treatment-related increases in multiple adenomas in both sexes
>>>>>>>>>>>>>>>>>>
BrooklynDodger(s) comment: This publication of an NTP study left the levels of evidence out of the abstract. These were "Under the conditions of these 2-year studies, there was some evidence of carcinogenic activity of methyl isobutyl ketone in male F344/N rats based on increased incidences of renal tubule neoplasms. Increased incidences of mononuclear cell leukemia in 1,800 ppm male F344/N rats may have been related to methyl isobutyl ketone exposure. There was equivocal evidence of carcinogenic activity of methyl isobutyl ketone in female F344/N rats based on the occurrence of renal mesenchymal tumors in the 1,800 ppm group. There was some evidence of carcinogenic activity of methyl isobutyl ketone in male and female B6C3F1 mice based on increased incidences of liver neoplasms." "Some" evidence is a study finding associations. The nephropathy in female rats undermines the Houdini alpha-2 theory. Liver tumors in both genders of mice is a strong finding. The Dodger(s) would add these findings up to a solid 2B carcinogen at IARC, or reasonably anticipated for the ROC. This is a rare organic vapor that didn't cause lung tumors in mice.
Sunday, March 08, 2009
A Trace of Information About Laptop Ergonomics
Applied ErgonomicsVolume 40, Issue 3, May 2009, Pages 404-409
University students’ notebook computer use
Karen Jacobsa, , , Peter Johnsonb, Jack Dennerleinc, Denise Petersond, Justin Kaufmane, Joshua Goldf, Sarah Williamsg, Nancy Richmondh, Stephanie Karbana, Emily Firna, Elizabeth Ansongd, Sarah Hudaka, Katherine Tungd, Victoria Halle, Karol Pencinai and Michael Pencinai
aBoston University, Sargent College, Department of Occupational Therapy, 635 Commonwealth Avenue, Boston, MA 02215, USA
bUniversity of Washington, School of Public Health and Community Medicine, Box 357230, Seattle, WA 98195-7230, USA
cHarvard University, School of Public Health, Landmark 404L, 665 Huntington Ave. Boston, MA 02115, USA
dBoston University, Sargent College, Department of Physical Therapy and Athletic Training, 635 Commonwealth Avenue, Boston, MA 02215, USA
eBoston University, College of Arts and Sciences, 725 Commonwealth Avenue, Boston, MA 02115, USA
fBoston University, Metropolitan College, 755 Commonwealth Avenue, Boston, MA 02115, USA
gBoston University, School of Education, 2 Sherborn Street, Boston, MA 02115, USA
hNortheastern University, Career Services, 360 Huntington Avenue, Boston, MA 02115, USA
iBoston University, School of Arts and Sciences, Department of Mathematics and Statistics, 704 Commonwealth Avenue, Boston, MA 02215, USA
Recent evidence suggests that university students are self-reporting experiencing musculoskeletal discomfort with computer use similar to levels reported by adult workers. The objective of this study was to determine how university students use notebook computers and to determine what ergonomic strategies might be effective in reducing self-reported musculoskeletal discomfort in this population. Two hundred and eighty-nine university students randomly assigned to one of three towers by the university's Office of Housing participated in this study. The results of this investigation showed a significant reduction in self-reported notebook computer-related discomfort from pre- and post-survey in participants who received notebook computer accessories and in those who received accessories and participatory ergonomics training. A significant increase in post-survey rest breaks was seen. There was a significant correlation between self-reported computer usage and the amount measured using computer usage software (odometer). More research is needed however to determine the most effective ergonomics intervention for university students.
>>>>>>>>>>>>>>>>>>>>>
BrooklynDodger(s) comment: There are certainly enough authors on this paper, which seems to involve half the schools in Boston. Looks like a 3 arm study, where the two interventions reduced discomfort. Looks like even the survey without the invervention changed behavior.
University students’ notebook computer use
Karen Jacobsa, , , Peter Johnsonb, Jack Dennerleinc, Denise Petersond, Justin Kaufmane, Joshua Goldf, Sarah Williamsg, Nancy Richmondh, Stephanie Karbana, Emily Firna, Elizabeth Ansongd, Sarah Hudaka, Katherine Tungd, Victoria Halle, Karol Pencinai and Michael Pencinai
aBoston University, Sargent College, Department of Occupational Therapy, 635 Commonwealth Avenue, Boston, MA 02215, USA
bUniversity of Washington, School of Public Health and Community Medicine, Box 357230, Seattle, WA 98195-7230, USA
cHarvard University, School of Public Health, Landmark 404L, 665 Huntington Ave. Boston, MA 02115, USA
dBoston University, Sargent College, Department of Physical Therapy and Athletic Training, 635 Commonwealth Avenue, Boston, MA 02215, USA
eBoston University, College of Arts and Sciences, 725 Commonwealth Avenue, Boston, MA 02115, USA
fBoston University, Metropolitan College, 755 Commonwealth Avenue, Boston, MA 02115, USA
gBoston University, School of Education, 2 Sherborn Street, Boston, MA 02115, USA
hNortheastern University, Career Services, 360 Huntington Avenue, Boston, MA 02115, USA
iBoston University, School of Arts and Sciences, Department of Mathematics and Statistics, 704 Commonwealth Avenue, Boston, MA 02215, USA
Recent evidence suggests that university students are self-reporting experiencing musculoskeletal discomfort with computer use similar to levels reported by adult workers. The objective of this study was to determine how university students use notebook computers and to determine what ergonomic strategies might be effective in reducing self-reported musculoskeletal discomfort in this population. Two hundred and eighty-nine university students randomly assigned to one of three towers by the university's Office of Housing participated in this study. The results of this investigation showed a significant reduction in self-reported notebook computer-related discomfort from pre- and post-survey in participants who received notebook computer accessories and in those who received accessories and participatory ergonomics training. A significant increase in post-survey rest breaks was seen. There was a significant correlation between self-reported computer usage and the amount measured using computer usage software (odometer). More research is needed however to determine the most effective ergonomics intervention for university students.
>>>>>>>>>>>>>>>>>>>>>
BrooklynDodger(s) comment: There are certainly enough authors on this paper, which seems to involve half the schools in Boston. Looks like a 3 arm study, where the two interventions reduced discomfort. Looks like even the survey without the invervention changed behavior.
Saturday, March 07, 2009
Danger of Benzene in the Street
Toxicology LettersVolume 181, Issue 1, 10 September 2008, Pages 25-30
Biological monitoring of low benzene exposure in Italian traffic policemen
Paola Maninia, b, , , Giuseppe De Palmac, Roberta Andreolia, b, Diana Polib, Marta Petyxd, Massimo Corradia, Antonio Muttia and Pietro Apostolic
aLaboratory of Industrial Toxicology, Department of Clinical Medicine, Nephrology and Health Sciences, University of Parma, Via Gramsci 14, 43100 Parma, Italy
bISPESL-National Institute for Occupational Safety and Prevention, Research Center at the University of Parma, Via Gramsci 14, 43100 Parma, Italy
cDepartment of Experimental and Applied Medicine, Occupational Medicine and Industrial Hygiene, University of Brescia, Piazzale Spedali Civili 1, 25123 Brescia, Italy
dISPESL-National Institute for Occupational Safety and Prevention, Department of Occupational Medicine, Via di Fontana Candida, 00141Monteporzio Catone, Rome, Italy
Abstract
A comparative evaluation of urinary biomarkers was carried out to characterize benzene exposure in a group of 100 traffic policemen of the city of Parma (Italy). All subjects were monitored once, in two consecutive days characterized by similar climatic conditions but preceded by two windy days. Benzene ambient concentration measured by municipal air monitoring stations was 1 μg/m3 (Day 1) and 2 μg/m3 (Day 2). Personal exposure to ambient concentrations of benzene, toluene, ethylbenzene and xylene (BTEX) was assessed by using Radiello® passive-diffusive samplers in a subgroup of 24 workers. Benzene metabolites, t,t-muconic acid (t,t-MA) and S-phenylmercapturic acid (S-PMA) were determined by isotopic dilution liquid chromatography–tandem mass spectrometry on spot urine samples collected at the end of the shift. Urinary benzene (U-B) was determined by solid-phase microextraction gas chromatography–mass spectrometry. Airborne benzene concentration expressed as median [and interquartile range] was 6.07 [0.28–9.53] μg/m3, as assessed by personal sampling. Urinary concentrations of biomarkers in the whole group were 41.8 [34.1–89.8] μg/g creatinine for t,t-MA, 0.67 [0.23–1.32] μg/g creatinine for S-PMA, and 0.16 [0.13–0.26] μg/l for U-B. Smokers eliminated significantly higher concentrations of unchanged BTEX and benzene metabolites than non-smokers (p < n =" 31)" p =" 0.003,">>>>>>>>>>>>>>>>>>>>>
BrooklynDodger(s) comment: The investigators were interested in the biomonitoring, but the Dodger(s) is(are) interested in how much benzene vapor was in the air on the average. The median exposure, converted to the ppm units for vapor exposures, was about .002 ppm or 2 pbb. EPA risk estimate, based on a Crump estimate in 1994, puts this risk somewhere above 1/100,000 and less than 1/10,000. The Dodger(s) isn't(aren't) sure whether more recent mortality studies wouldn't push the risk higher
Biological monitoring of low benzene exposure in Italian traffic policemen
Paola Maninia, b, , , Giuseppe De Palmac, Roberta Andreolia, b, Diana Polib, Marta Petyxd, Massimo Corradia, Antonio Muttia and Pietro Apostolic
aLaboratory of Industrial Toxicology, Department of Clinical Medicine, Nephrology and Health Sciences, University of Parma, Via Gramsci 14, 43100 Parma, Italy
bISPESL-National Institute for Occupational Safety and Prevention, Research Center at the University of Parma, Via Gramsci 14, 43100 Parma, Italy
cDepartment of Experimental and Applied Medicine, Occupational Medicine and Industrial Hygiene, University of Brescia, Piazzale Spedali Civili 1, 25123 Brescia, Italy
dISPESL-National Institute for Occupational Safety and Prevention, Department of Occupational Medicine, Via di Fontana Candida, 00141Monteporzio Catone, Rome, Italy
Abstract
A comparative evaluation of urinary biomarkers was carried out to characterize benzene exposure in a group of 100 traffic policemen of the city of Parma (Italy). All subjects were monitored once, in two consecutive days characterized by similar climatic conditions but preceded by two windy days. Benzene ambient concentration measured by municipal air monitoring stations was 1 μg/m3 (Day 1) and 2 μg/m3 (Day 2). Personal exposure to ambient concentrations of benzene, toluene, ethylbenzene and xylene (BTEX) was assessed by using Radiello® passive-diffusive samplers in a subgroup of 24 workers. Benzene metabolites, t,t-muconic acid (t,t-MA) and S-phenylmercapturic acid (S-PMA) were determined by isotopic dilution liquid chromatography–tandem mass spectrometry on spot urine samples collected at the end of the shift. Urinary benzene (U-B) was determined by solid-phase microextraction gas chromatography–mass spectrometry. Airborne benzene concentration expressed as median [and interquartile range] was 6.07 [0.28–9.53] μg/m3, as assessed by personal sampling. Urinary concentrations of biomarkers in the whole group were 41.8 [34.1–89.8] μg/g creatinine for t,t-MA, 0.67 [0.23–1.32] μg/g creatinine for S-PMA, and 0.16 [0.13–0.26] μg/l for U-B. Smokers eliminated significantly higher concentrations of unchanged BTEX and benzene metabolites than non-smokers (p < n =" 31)" p =" 0.003,">>>>>>>>>>>>>>>>>>>>>
BrooklynDodger(s) comment: The investigators were interested in the biomonitoring, but the Dodger(s) is(are) interested in how much benzene vapor was in the air on the average. The median exposure, converted to the ppm units for vapor exposures, was about .002 ppm or 2 pbb. EPA risk estimate, based on a Crump estimate in 1994, puts this risk somewhere above 1/100,000 and less than 1/10,000. The Dodger(s) isn't(aren't) sure whether more recent mortality studies wouldn't push the risk higher
Friday, March 06, 2009
Arsenic and Old Glutathione - Insights into Exposure Response or Houdini Alert?
Toxicol. Sci. 2009 107: 309-311; doi:10.1093/toxsci/kfn257.
http://toxsci.oxfordjournals.org/cgi/content/full/107/2/309?etoc
Unraveling Arsenic—Glutathione Connections
David J. Thomas1
Pharmacokinetics Branch, Experimental Toxicology Division, National Health and Environmental Effects Research Laboratory, Office of Research and Development, MD B143-1, U.S. Environmental Protection Agency, 109 Alexander Drive, Research Triangle Park, North Carolina 27711
1 For correspondence via fax: 919-541-1937. E-mail: thomas.david@epa.gov
The paper by Muniz Ortiz et al. (2009) in this issue of Toxicological Sciences extends a long line of research on the role of glutathione (GSH) in the metabolism and toxicity of arsenic (As). These investigators used Drosophila as their model organism and the tools of classical and molecular genetics to investigate the genetic basis of variation in sensitivity to the toxic effects of inorganic As. By measuring eclosion (egg hatching) rates for different Drosophila strains cultured on arsenite-containing medium, they identified strains that differed manyfold in sensitivity to As. Using As-sensitive or -resistant strains, they showed an As-resistant phenotype to be related to the genotype for glutathione synthetase (GS). The GS gene encodes the enzyme that catalyzes the second and final step in a pathway that produces GSH from its constituent amino acids. Armed with this information, they used RNA interference to show that altered expression of the GS gene affects sensitivity to As in cultured cells and in flies. Taken in sum, these results emphasize the potential importance of GS genotype that determines the capacity to produce GSH in determining the phenotype for sensitivity to the toxic and carcinogenic effects of As.
To appreciate the significance of this research, it is useful to consider the context in which this research developed, our current knowledge of the linkages between As and GSH metabolism, and the prospects for future research to elucidate this relation.
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BrooklynDodger(s) Comments: Shame on the reviewers for not forcing text clarity on whether more GSH increases resistance. Let's assume it does. GST variation is increasingly competing with CYP variation as a hypothesis for explaining toxic potency variation across individuals and species. While GST is classed as a Type II enzyme in most texts, the Dodger(s) think(s) it's more a Type I attacking either the primary agent or a proximal toxicant, dealkylating the agent to a polar form rather than conjugating to a polar form. The Dodger(s) is(are) unconvinced that the short time exposure effects observed here and in other studies have been demonstrated in chronic exposure scenarios (either for GST or CYP).
The Dodger(s) note(s) that increased GST activity in mouse lung is claimed to explain reduced resistance in mice to the lung carcinogenicity of inhaled methylene chloride. This is the basis for the "mouse clara cell" houdini risk assessment of methylene chloride.
http://toxsci.oxfordjournals.org/cgi/content/full/107/2/309?etoc
Unraveling Arsenic—Glutathione Connections
David J. Thomas1
Pharmacokinetics Branch, Experimental Toxicology Division, National Health and Environmental Effects Research Laboratory, Office of Research and Development, MD B143-1, U.S. Environmental Protection Agency, 109 Alexander Drive, Research Triangle Park, North Carolina 27711
1 For correspondence via fax: 919-541-1937. E-mail: thomas.david@epa.gov
The paper by Muniz Ortiz et al. (2009) in this issue of Toxicological Sciences extends a long line of research on the role of glutathione (GSH) in the metabolism and toxicity of arsenic (As). These investigators used Drosophila as their model organism and the tools of classical and molecular genetics to investigate the genetic basis of variation in sensitivity to the toxic effects of inorganic As. By measuring eclosion (egg hatching) rates for different Drosophila strains cultured on arsenite-containing medium, they identified strains that differed manyfold in sensitivity to As. Using As-sensitive or -resistant strains, they showed an As-resistant phenotype to be related to the genotype for glutathione synthetase (GS). The GS gene encodes the enzyme that catalyzes the second and final step in a pathway that produces GSH from its constituent amino acids. Armed with this information, they used RNA interference to show that altered expression of the GS gene affects sensitivity to As in cultured cells and in flies. Taken in sum, these results emphasize the potential importance of GS genotype that determines the capacity to produce GSH in determining the phenotype for sensitivity to the toxic and carcinogenic effects of As.
To appreciate the significance of this research, it is useful to consider the context in which this research developed, our current knowledge of the linkages between As and GSH metabolism, and the prospects for future research to elucidate this relation.
>>>>>>>>>>>>>>>>>>>>
BrooklynDodger(s) Comments: Shame on the reviewers for not forcing text clarity on whether more GSH increases resistance. Let's assume it does. GST variation is increasingly competing with CYP variation as a hypothesis for explaining toxic potency variation across individuals and species. While GST is classed as a Type II enzyme in most texts, the Dodger(s) think(s) it's more a Type I attacking either the primary agent or a proximal toxicant, dealkylating the agent to a polar form rather than conjugating to a polar form. The Dodger(s) is(are) unconvinced that the short time exposure effects observed here and in other studies have been demonstrated in chronic exposure scenarios (either for GST or CYP).
The Dodger(s) note(s) that increased GST activity in mouse lung is claimed to explain reduced resistance in mice to the lung carcinogenicity of inhaled methylene chloride. This is the basis for the "mouse clara cell" houdini risk assessment of methylene chloride.
Thursday, March 05, 2009
Female Gender and Increased Injury Risk
American Journal of Epidemiology 2009 169(2):161-166; doi:10.1093/aje/kwn304
Sex Differences in Injury Patterns Among Workers in Heavy Manufacturing
Oyebode A. Taiwo, Linda F. Cantley, Martin D. Slade, Keshia M. Pollack, Sally Vegso, Martha G. Fiellin and Mark R. Cullen
Correspondence to Martha G. Fiellin, Yale Occupational and Environmental Medicine Program, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT (e-mail: martha.fiellin@yale.edu
The objective of the study was to determine if female workers in a heavy manufacturing environment have a higher risk of injury compared with males when performing the same job and to evaluate sex differences in type or severity of injury. By use of human resources and incident surveillance data for the hourly population at 6 US aluminum smelters, injuries that occurred from January 1, 1996, through December 21, 2005, were analyzed. Multivariate logistic regression, adjusted for job, tenure, and age category, was used to calculate odds ratios and 95% confidence intervals for female versus male injury risk for all injuries, recordable injuries, and lost work time injuries. The analysis was repeated for acute injuries and musculoskeletal disorder-related injuries separately. Female workers in this industry have a greater risk for sustaining all forms of injury after adjustment for age, tenure, and standardized job category (odds ratio = 1.365, 95% confidence interval: 1.290, 1.445). This excess risk for female workers persisted when injuries were dichotomized into acute injuries (odds ratio = 1.2) and musculoskeletal disorder-related injuries (odds ratio = 1.1). This study provides evidence of a sex disparity in occupational injury with female workers at higher risk compared with their male counterparts in a heavy manufacturing environment.
Sex Differences in Injury Patterns Among Workers in Heavy Manufacturing
Oyebode A. Taiwo, Linda F. Cantley, Martin D. Slade, Keshia M. Pollack, Sally Vegso, Martha G. Fiellin and Mark R. Cullen
Correspondence to Martha G. Fiellin, Yale Occupational and Environmental Medicine Program, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT (e-mail: martha.fiellin@yale.edu
The objective of the study was to determine if female workers in a heavy manufacturing environment have a higher risk of injury compared with males when performing the same job and to evaluate sex differences in type or severity of injury. By use of human resources and incident surveillance data for the hourly population at 6 US aluminum smelters, injuries that occurred from January 1, 1996, through December 21, 2005, were analyzed. Multivariate logistic regression, adjusted for job, tenure, and age category, was used to calculate odds ratios and 95% confidence intervals for female versus male injury risk for all injuries, recordable injuries, and lost work time injuries. The analysis was repeated for acute injuries and musculoskeletal disorder-related injuries separately. Female workers in this industry have a greater risk for sustaining all forms of injury after adjustment for age, tenure, and standardized job category (odds ratio = 1.365, 95% confidence interval: 1.290, 1.445). This excess risk for female workers persisted when injuries were dichotomized into acute injuries (odds ratio = 1.2) and musculoskeletal disorder-related injuries (odds ratio = 1.1). This study provides evidence of a sex disparity in occupational injury with female workers at higher risk compared with their male counterparts in a heavy manufacturing environment.
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BrooklynDodger(s) Comment: Finding a 37% excess risk among women carries some political implications, although this is not much of a difference given the nature of OSHA based statistics. Any of these rates is sensitive to propensity to record and propensity to report. Which goes back to facility culture. This report is pretty clearly about Alcoa. Stratification of injuries by nature - MSD v. acute - and of victims by job class is very sophisticated. Some of the numbers don't add up: injuries are stratified into MSD and acute [very sophisticated] but the relative risk for each is less than the relative risk combined. Maybe there's an "other category"?
Wednesday, March 04, 2009
Job Content of Intensive Care Nursing
Applied ErgonomicsVolume 40, Issue 3, May 2009, Pages 509-518
Exploring performance obstacles of intensive care nurses
Ayse P. Gursesa, , and Pascale Carayonb, 1,
aJohns Hopkins University School of Medicine, Department of Anesthesiology and Critical Care Medicine, Quality & Safety Research Group, 1909 Thames Street - 1st Floor, Baltimore, MD, 21231, United States
bDepartment of Industrial and Systems Engineering, Center for Quality and Productivity Improvement, University of Wisconsin-Madison, 1550 Engineering Drive, 3126 Engineering Centers Building, Madison, WI, 53706, United States
High nursing workload, poor patient safety, and poor nursing quality of working life (QWL) are major issues in intensive care units (ICUs). Characteristics of the ICU and performance obstacles may contribute to these issues. The goal of this study was to comprehensively identify the performance obstacles perceived by ICU nurses. We used a qualitative research design and conducted semi-structured interviews with 15 ICU nurses of a medical-surgical ICU. Based on this qualitative study and a previously reported quantitative study, we identified seven main types of performance obstacles experienced by ICU nurses. Obstacles related to the physical environment (e.g., noise, amount of space), family relations (e.g., distractions caused by family, lack of time to spend with family), and equipment (e.g., unavailability, misplacement) were the most frequently experienced performance obstacles. The qualitative interview data provided rich information regarding the factors contributing to the performance obstacles. Overall, ICU nurses experience a variety of performance obstacles in their work on a daily basis. Future research is needed to understand the impact of performance obstacles on nursing workload, nursing QWL, and quality and safety of care.
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BrooklynDodger(s) comment: The Dodger(s) wonder(s) if this is a part of a doctoral project, the whole project, a masters project, or what. Descriptive information is always helpful in shaping further research. In this case, comparison with other nursing environment would lead to some conclusions about impact of work environment in ICU. The Dodger(s) has(have) often opined that if you wanted to design work organization to create medical errors, you'd get pretty much what now exists in the health care system. The Dodger(s) is(are) glad to see an ergonomics journal address health care.
Exploring performance obstacles of intensive care nurses
Ayse P. Gursesa, , and Pascale Carayonb, 1,
aJohns Hopkins University School of Medicine, Department of Anesthesiology and Critical Care Medicine, Quality & Safety Research Group, 1909 Thames Street - 1st Floor, Baltimore, MD, 21231, United States
bDepartment of Industrial and Systems Engineering, Center for Quality and Productivity Improvement, University of Wisconsin-Madison, 1550 Engineering Drive, 3126 Engineering Centers Building, Madison, WI, 53706, United States
High nursing workload, poor patient safety, and poor nursing quality of working life (QWL) are major issues in intensive care units (ICUs). Characteristics of the ICU and performance obstacles may contribute to these issues. The goal of this study was to comprehensively identify the performance obstacles perceived by ICU nurses. We used a qualitative research design and conducted semi-structured interviews with 15 ICU nurses of a medical-surgical ICU. Based on this qualitative study and a previously reported quantitative study, we identified seven main types of performance obstacles experienced by ICU nurses. Obstacles related to the physical environment (e.g., noise, amount of space), family relations (e.g., distractions caused by family, lack of time to spend with family), and equipment (e.g., unavailability, misplacement) were the most frequently experienced performance obstacles. The qualitative interview data provided rich information regarding the factors contributing to the performance obstacles. Overall, ICU nurses experience a variety of performance obstacles in their work on a daily basis. Future research is needed to understand the impact of performance obstacles on nursing workload, nursing QWL, and quality and safety of care.
>>>>>>>>>>>>>>>>>
BrooklynDodger(s) comment: The Dodger(s) wonder(s) if this is a part of a doctoral project, the whole project, a masters project, or what. Descriptive information is always helpful in shaping further research. In this case, comparison with other nursing environment would lead to some conclusions about impact of work environment in ICU. The Dodger(s) has(have) often opined that if you wanted to design work organization to create medical errors, you'd get pretty much what now exists in the health care system. The Dodger(s) is(are) glad to see an ergonomics journal address health care.
Tuesday, March 03, 2009
Fullerene Inhalation Impacts Immune Response - Another Nanoparticle Hazard ID
ToxicologyVolume 258, Issue 1, 5 April 2009, Pages 47-55
Gene expression profiles in rat lung after inhalation exposure to C60 fullerene particles
Katsuhide Fujitaa, , , Yasuo Morimotob, Akira Ogamib, Toshihiko Myojyob, Isamu Tanakab, Manabu Shimadac, Wei-Ning Wangc, Shigehisa Endohd, Kunio Uchidad, Tetsuya Nakazatod, Kazuhiro Yamamotoe, Hiroko Fukuia, Masanori Horiea, Yasukazu Yoshidaa, Hitoshi Iwahashia and Junko Nakanishif
aHealth Technology Research Center, National Institute of Advanced Industrial Science and Technology (AIST), Onogawa 16-1, Tsukuba, Ibaraki 305-8569, Japan
bInstitute of Industrial Ecological Sciences, University of Occupational and Environmental Health, Kitakyushu 807-8555, Japan
cGraduate School of Engineering, Hiroshima University, Higashi Hiroshima 739-8527, Japan
dResearch Institute for Environmental Management Technology, National Institute of Advanced Industrial Science and Technology (AIST), Tsukuba 305-8569, Japan
eResearch Institute of Instrumentation Frontier, National Institute of Advanced Industrial Science and Technology (AIST), Tsukuba 305-8568, Japan
fResearch Institute of Science for Safety and Sustainability, National Institute of Advanced Industrial Science and Technology (AIST), Tsukuba 305-8569, Japan
Abstract
Concern over the influence of nanoparticles on human health has risen due to advances in the development of nanotechnology. We are interested in the influence of nanoparticles on the pulmonary system at a molecular level. In this study, gene expression profiling of the rat lung after whole-body inhalation exposure to C60 fullerene (0.12 mg/m3; 4.1 × 104 particles/cm3, 96 nm diameter) and ultrafine nickel oxide (Uf-NiO) particles (0.2 mg/m3; 9.2 × 104 particles/cm3, 59 nm diameter) as a positive control were employed to gain insights into these molecular events. In response to C60 fullerene exposure for 6 h a day, for 4 weeks (5 days a week), C60 fullerene particles were located in alveolar epithelial cells at 3 days post-exposure and engulfed by macrophages at both 3 days and 1 month post-exposures. Gene expression profiles revealed that few genes involved in the inflammatory response, oxidative stress, apoptosis, and metalloendopeptidase activity were up-regulated at both 3 days and 1 month post-exposure. Only some genes associated with the immune system process, including major histocompatibility complex (MHC)-mediated immunity were up-regulated. These results were significantly different from those of Uf-NiO particles which induced high expression of genes associated with chemokines, oxidative stress, and matrix metalloproteinase 12 (Mmp12), suggesting that Uf-NiO particles lead to acute inflammation for the inhalation exposure period, and the damaged tissues were repaired in the post-exposure period. We suggest that C60 fullerene might not have a severe pulmonary toxicity under the inhalation exposure condition.
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BrooklynDodger(s) comment: There's a bit of "don't worry, be happy" in the final conclusion here. Fullerenes are really high tech carbon black, and carbon black is a 2A carcinogen. The study indicates that inhalation at 120 ug/cm3 affects immune response, but doesn't have the inflammatory response of nickel oxide, also a carcinogen. But, the nickel oxide exposure involved substantially more mass, more than twice the particle number, and substantially smaller particles. It would have been better to include an ultrafine carbon black to determine whether there was a differential with fullerenes.
Gene expression profiles in rat lung after inhalation exposure to C60 fullerene particles
Katsuhide Fujitaa, , , Yasuo Morimotob, Akira Ogamib, Toshihiko Myojyob, Isamu Tanakab, Manabu Shimadac, Wei-Ning Wangc, Shigehisa Endohd, Kunio Uchidad, Tetsuya Nakazatod, Kazuhiro Yamamotoe, Hiroko Fukuia, Masanori Horiea, Yasukazu Yoshidaa, Hitoshi Iwahashia and Junko Nakanishif
aHealth Technology Research Center, National Institute of Advanced Industrial Science and Technology (AIST), Onogawa 16-1, Tsukuba, Ibaraki 305-8569, Japan
bInstitute of Industrial Ecological Sciences, University of Occupational and Environmental Health, Kitakyushu 807-8555, Japan
cGraduate School of Engineering, Hiroshima University, Higashi Hiroshima 739-8527, Japan
dResearch Institute for Environmental Management Technology, National Institute of Advanced Industrial Science and Technology (AIST), Tsukuba 305-8569, Japan
eResearch Institute of Instrumentation Frontier, National Institute of Advanced Industrial Science and Technology (AIST), Tsukuba 305-8568, Japan
fResearch Institute of Science for Safety and Sustainability, National Institute of Advanced Industrial Science and Technology (AIST), Tsukuba 305-8569, Japan
Abstract
Concern over the influence of nanoparticles on human health has risen due to advances in the development of nanotechnology. We are interested in the influence of nanoparticles on the pulmonary system at a molecular level. In this study, gene expression profiling of the rat lung after whole-body inhalation exposure to C60 fullerene (0.12 mg/m3; 4.1 × 104 particles/cm3, 96 nm diameter) and ultrafine nickel oxide (Uf-NiO) particles (0.2 mg/m3; 9.2 × 104 particles/cm3, 59 nm diameter) as a positive control were employed to gain insights into these molecular events. In response to C60 fullerene exposure for 6 h a day, for 4 weeks (5 days a week), C60 fullerene particles were located in alveolar epithelial cells at 3 days post-exposure and engulfed by macrophages at both 3 days and 1 month post-exposures. Gene expression profiles revealed that few genes involved in the inflammatory response, oxidative stress, apoptosis, and metalloendopeptidase activity were up-regulated at both 3 days and 1 month post-exposure. Only some genes associated with the immune system process, including major histocompatibility complex (MHC)-mediated immunity were up-regulated. These results were significantly different from those of Uf-NiO particles which induced high expression of genes associated with chemokines, oxidative stress, and matrix metalloproteinase 12 (Mmp12), suggesting that Uf-NiO particles lead to acute inflammation for the inhalation exposure period, and the damaged tissues were repaired in the post-exposure period. We suggest that C60 fullerene might not have a severe pulmonary toxicity under the inhalation exposure condition.
>>>>>>>>>>>>>>>>>>>
BrooklynDodger(s) comment: There's a bit of "don't worry, be happy" in the final conclusion here. Fullerenes are really high tech carbon black, and carbon black is a 2A carcinogen. The study indicates that inhalation at 120 ug/cm3 affects immune response, but doesn't have the inflammatory response of nickel oxide, also a carcinogen. But, the nickel oxide exposure involved substantially more mass, more than twice the particle number, and substantially smaller particles. It would have been better to include an ultrafine carbon black to determine whether there was a differential with fullerenes.
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