This is a study of normal healthy subjects exposed for a day at levels below the EPA single day limit, but above the EPA annual average. The 50 microgram exposure compares to the 5000 micrograms permitted by OSHA.
In this study, the subjects denied symptoms and didn’t express sputum, even though there were measurable deficits in lung function even a day after exposure. These findings demonstrate that symptoms, which are often observed in the absence of quantitative clinical findings, are not always the most sensitive indicator of toxic respiratory effects.
A summary of the abstract follows:
"Particulate air pollution is associated with asthma exacerbations and increased morbidity and mortality from respiratory causes. … Healthy subjects were exposed to carbon particle concentrations of 10, 25, and 50 microg/m(3), while asthmatics were exposed to 10 microg/m(3). … exposing 16 normal subjects to … 50 microg/m(3) caused a reduction in maximal midexpiratory flow rate … and carbon monoxide diffusing capacity … at 21 h after exposure. There were no consistent differences in symptoms…exposure to carbon ultrafine particles results in mild small-airways dysfunction together with impaired alveolar gas exchange in normal subjects. These effects do not appear related to airway inflammation…"
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Inhal Toxicol. 2004;16 Suppl 1:59-72.
Pulmonary function, diffusing capacity, and inflammation in healthy and asthmatic subjects exposed to ultrafine particles.
Pietropaoli AP, Frampton MW, Hyde RW, Morrow PE, Oberdorster G, Cox C, Speers DM, Frasier LM, Chalupa DC, Huang LS, Utell MJ.Department of Medicine, University of Rochester School of Medicine and Dentistry, New York 14642, USA. Anthony_Pietropaoli@urmc.rochester.edu
Particulate air pollution is associated with asthma exacerbations and increased morbidity and mortality from respiratory causes. Ultrafine particles (particles less than 0.1 microm in diameter) may contribute to these adverse effects because they have a higher predicted pulmonary deposition, greater potential to induce pulmonary inflammation, larger surface area, and enhanced oxidant capacity when compared with larger particles on a mass basis. We hypothesized that ultrafine particle exposure would induce airway inflammation in susceptible humans. This hypothesis was tested in a series of randomized, double-blind studies by exposing healthy subjects and mild asthmatic subjects to carbon ultrafine particles versus filtered air. Both exposures were delivered via a mouthpiece system during rest and moderate exercise. Healthy subjects were exposed to particle concentrations of 10, 25, and 50 microg/m(3), while asthmatics were exposed to 10 microg/m(3). Lung function and airway inflammation were assessed by symptom scores, pulmonary function tests, and airway nitric oxide parameters. Airway inflammatory cells were measured via induced sputum analysis in several of the protocols. There were no differences in any of these measurements in normal or asthmatic subjects when exposed to ultrafine particles at concentrations of 10 or 25 microg/m(3). However, exposing 16 normal subjects to the higher concentration of 50 microg/m(3) caused a reduction in maximal midexpiratory flow rate (-4.34 +/- 1.78% [ultrafine particles] vs. +1.08 +/- 1.86% [air], p =.042) and carbon monoxide diffusing capacity (-1.76 +/- 0.66 ml/min/mm Hg [ultrafine particles] vs. -0.18 +/- 0.41 ml/min/mm Hg [air], p =.040) at 21 h after exposure. There were no consistent differences in symptoms, induced sputum, or exhaled nitric oxide parameters in any of these studies. These results suggest that exposure to carbon ultrafine particles results in mild small-airways dysfunction together with impaired alveolar gas exchange in normal subjects. These effects do not appear related to airway inflammation. Additional studies are required to confirm these findings in normal subjects, compare them with additional susceptible patient populations, and determine their pathophysiologic mechanisms.
Sunday, February 27, 2005
Systemic Effects of short term inhalation of carbon at levels permitted by OSHA
Another laboratory study supports the observed cardiovascular toxicity of fine particles without other known toxicity. Carbon black is carcinogenic in the rat by inhalation. These exposure levels are about 1/3 of the OSHA limit for day in and day out exposure.
The condensed abstract notes:
…We hypothesized that inhaled ultrafine particles result in an inflammatory response which may stimulate systemic clotting factor release. … rats were exposed to either fine or ultrafine carbon black (CB) for 7 h. … total suspended particle concentrations were 1.66 mg/m(3) for ultrafine CB and 1.40 mg/m(3) for fine CB. Particle concentration of ultrafine particles was more than 10 times greater than that of fine particles… ultrafine CB caused an increase in total bronchoalveolar lavage (BAL) leukocytes… … Exposure to the ultrafine, but not fine, carbon was also associated with significant increases in the total numbers of blood leukocytes. … The data show that there is a small but consistent significant proinflammatory effect of this exposure to ultrafine particles that is greater than the effect of the same exposure to fine CB.
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Toxicol Appl Pharmacol. 2004 Feb 15;195(1):35-44.
Pulmonary and systemic effects of short-term inhalation exposure to ultrafine carbon black particles.
Gilmour PS, Ziesenis A, Morrison ER, Vickers MA, Drost EM, Ford I, Karg E, Mossa C, Schroeppel A, Ferron GA, Heyder J, Greaves M, MacNee W, Donaldson K.
Edinburgh Lung and the Environment Group Initiative (ELEGI)/Colt Laboratory, The MRC Centre for Inflammation Research, Medical School, The University of Edinburgh, Edinburgh EH8 9AG, UK.
While environmental particles are associated with mortality and morbidity related to pulmonary and cardiovascular (CV) disease, the mechanisms involved in CV health effects are not known. Changes in systemic clotting factors have been associated with pulmonary inflammation. We hypothesized that inhaled ultrafine particles result in an inflammatory response which may stimulate systemic clotting factor release. Adult male Wistar rats were exposed to either fine or ultrafine carbon black (CB) for 7 h. The attained total suspended particle concentrations were 1.66 mg/m(3) for ultrafine CB and 1.40 mg/m(3) for fine CB. Particle concentration of ultrafine particles was more than 10 times greater than that of fine particles and the count median aerodynamic diameter averaged 114 nm for the ultrafine and 268 nm for the fine carbon particles. Data were collected immediately, 16 and 48 h following exposure. Only ultrafine CB caused an increase in total bronchoalveolar lavage (BAL) leukocytes, whereas both fine (2-fold) and ultrafine (4-fold) carbon particles caused an increase in BAL neutrophils at 16 h postexposure. Exposure to the ultrafine, but not fine, carbon was also associated with significant increases in the total numbers of blood leukocytes. Plasma fibrinogen, factor VII and von Willebrand factor (vWF) were unaffected by particle treatments as was plasma Trolox equivalent antioxidant status (TEAC). Macrophage inflammatory protein-2 mRNA was significantly increased in BAL cells 48 h following exposure to ultrafine CB. The data show that there is a small but consistent significant proinflammatory effect of this exposure to ultrafine particles that is greater than the effect of the same exposure to fine CB.
The condensed abstract notes:
…We hypothesized that inhaled ultrafine particles result in an inflammatory response which may stimulate systemic clotting factor release. … rats were exposed to either fine or ultrafine carbon black (CB) for 7 h. … total suspended particle concentrations were 1.66 mg/m(3) for ultrafine CB and 1.40 mg/m(3) for fine CB. Particle concentration of ultrafine particles was more than 10 times greater than that of fine particles… ultrafine CB caused an increase in total bronchoalveolar lavage (BAL) leukocytes… … Exposure to the ultrafine, but not fine, carbon was also associated with significant increases in the total numbers of blood leukocytes. … The data show that there is a small but consistent significant proinflammatory effect of this exposure to ultrafine particles that is greater than the effect of the same exposure to fine CB.
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Toxicol Appl Pharmacol. 2004 Feb 15;195(1):35-44.
Pulmonary and systemic effects of short-term inhalation exposure to ultrafine carbon black particles.
Gilmour PS, Ziesenis A, Morrison ER, Vickers MA, Drost EM, Ford I, Karg E, Mossa C, Schroeppel A, Ferron GA, Heyder J, Greaves M, MacNee W, Donaldson K.
Edinburgh Lung and the Environment Group Initiative (ELEGI)/Colt Laboratory, The MRC Centre for Inflammation Research, Medical School, The University of Edinburgh, Edinburgh EH8 9AG, UK.
While environmental particles are associated with mortality and morbidity related to pulmonary and cardiovascular (CV) disease, the mechanisms involved in CV health effects are not known. Changes in systemic clotting factors have been associated with pulmonary inflammation. We hypothesized that inhaled ultrafine particles result in an inflammatory response which may stimulate systemic clotting factor release. Adult male Wistar rats were exposed to either fine or ultrafine carbon black (CB) for 7 h. The attained total suspended particle concentrations were 1.66 mg/m(3) for ultrafine CB and 1.40 mg/m(3) for fine CB. Particle concentration of ultrafine particles was more than 10 times greater than that of fine particles and the count median aerodynamic diameter averaged 114 nm for the ultrafine and 268 nm for the fine carbon particles. Data were collected immediately, 16 and 48 h following exposure. Only ultrafine CB caused an increase in total bronchoalveolar lavage (BAL) leukocytes, whereas both fine (2-fold) and ultrafine (4-fold) carbon particles caused an increase in BAL neutrophils at 16 h postexposure. Exposure to the ultrafine, but not fine, carbon was also associated with significant increases in the total numbers of blood leukocytes. Plasma fibrinogen, factor VII and von Willebrand factor (vWF) were unaffected by particle treatments as was plasma Trolox equivalent antioxidant status (TEAC). Macrophage inflammatory protein-2 mRNA was significantly increased in BAL cells 48 h following exposure to ultrafine CB. The data show that there is a small but consistent significant proinflammatory effect of this exposure to ultrafine particles that is greater than the effect of the same exposure to fine CB.
Co-Carcinogenic Effect of Vitamin A and C in Laboratory Studies
BrooklynDodger previously posted a mega chemoprevention study of Vitamin A in smokers and asbestos workers in which the vitamins were was stopped in mid stream as it became evident that there was increased cancer in the vitamin treated patients. [The non treatment arm of the study in asbestos workers provided useful information about the natural history of disease among those people. BrooklynDodger will return to that in another post.]
Now comes a laboratory study which duplicates this effect in guinea pigs. The abstract is paraphrased here and repeated in full below:
…guinea pigs treated with cigarette smoke by inhalation twice a day for 28 days developed preneoplastic lung lesions, including bronchial hyperplasia, dysplasia and squamous metaplasia, analogous to those found in human smokers. …Compared with a diet low in vitamin C …and vitamin E …, a diet high in vitamin C … and vitamin E … significantly increased the incidence of these lesions. … As in human smokers, levels of ascorbate in blood plasma, lung, liver and the adrenal glands were significantly decreased by cigarette smoke inhalation. These results … provide additional evidence that very high dietary levels of certain antioxidants can have co-carcinogenic activity in cigarette smoke-induced lung cancer.
Probably this applies to all environmental risks for lung cancer, fine particles as well as asbestos. The “healthy” diet promoted by the blame the victim establishment increases risk. Nothing to be done but prevent the exposures.
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Carcinogenesis 2005 26(3):605-612; doi:10.1093/carcin/bgh341
Induction of preneoplastic lung lesions in guinea pigs by cigarette smoke inhalation and their exacerbation by high dietary levels of vitamins C and E
Emerich S. Fiala2, Ock Soon Sohn, Chung-Xiou Wang, Eleanore Seibert, Junji Tsurutani1, Phillip A. Dennis1, Karam El-Bayoumy, Rama S. Sodum, Dhimant Desai, Joel Reinhardt and Cesar Aliaga
Institute for Cancer Prevention, Valhalla, NY, USA and 1 Cancer Therapeutics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA
The development of effective chemopreventive agents against cigarette smoke-induced lung cancer could be greatly facilitated by the availability of suitable laboratory animal models. Here we report that male Hartley guinea pigs treated with cigarette smoke by inhalation twice a day for 28 days developed preneoplastic lung lesions, including bronchial hyperplasia, dysplasia and squamous metaplasia, analogous to those found in human smokers. The lesions were accompanied by increased expression of proliferating cell nuclear antigen and activation of the serine/threonine kinase Akt in the bronchial epithelium. In contrast, no lung lesions were found in guinea pigs (‘sham smoked’) that were submitted to identical procedures but without cigarettes. Compared with a diet low in vitamin C (50 p.p.m.) and vitamin E (15 p.p.m.), a diet high in vitamin C (4000 p.p.m.) and vitamin E (40 p.p.m.) significantly increased the incidence of these lesions. The inclusion of 1,4-phenylenebis(methylene)selenocyanate (p-XSC), a synthetic chemopreventive organoselenium compound, in the high vitamin C–high vitamin E diet at a level of 15 p.p.m. as selenium appeared to decrease the lesion incidence. Administration of (–)-epigallocatechin gallate, a powerful green tea polyphenolic antioxidant, at 560 p.p.m. in the drinking water had no effect. As in human smokers, levels of ascorbate in blood plasma, lung, liver and the adrenal glands were significantly decreased by cigarette smoke inhalation. These results identify a relevant in vivo laboratory model of cigarette smoke-induced lung cancer, suggest that p-XSC may have activity as a chemopreventive agent against cigarette smoke-induced lung lesions and provide additional evidence that very high dietary levels of certain antioxidants can have co-carcinogenic activity in cigarette smoke-induced lung cancer.
Now comes a laboratory study which duplicates this effect in guinea pigs. The abstract is paraphrased here and repeated in full below:
…guinea pigs treated with cigarette smoke by inhalation twice a day for 28 days developed preneoplastic lung lesions, including bronchial hyperplasia, dysplasia and squamous metaplasia, analogous to those found in human smokers. …Compared with a diet low in vitamin C …and vitamin E …, a diet high in vitamin C … and vitamin E … significantly increased the incidence of these lesions. … As in human smokers, levels of ascorbate in blood plasma, lung, liver and the adrenal glands were significantly decreased by cigarette smoke inhalation. These results … provide additional evidence that very high dietary levels of certain antioxidants can have co-carcinogenic activity in cigarette smoke-induced lung cancer.
Probably this applies to all environmental risks for lung cancer, fine particles as well as asbestos. The “healthy” diet promoted by the blame the victim establishment increases risk. Nothing to be done but prevent the exposures.
>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
Carcinogenesis 2005 26(3):605-612; doi:10.1093/carcin/bgh341
Induction of preneoplastic lung lesions in guinea pigs by cigarette smoke inhalation and their exacerbation by high dietary levels of vitamins C and E
Emerich S. Fiala2, Ock Soon Sohn, Chung-Xiou Wang, Eleanore Seibert, Junji Tsurutani1, Phillip A. Dennis1, Karam El-Bayoumy, Rama S. Sodum, Dhimant Desai, Joel Reinhardt and Cesar Aliaga
Institute for Cancer Prevention, Valhalla, NY, USA and 1 Cancer Therapeutics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA
The development of effective chemopreventive agents against cigarette smoke-induced lung cancer could be greatly facilitated by the availability of suitable laboratory animal models. Here we report that male Hartley guinea pigs treated with cigarette smoke by inhalation twice a day for 28 days developed preneoplastic lung lesions, including bronchial hyperplasia, dysplasia and squamous metaplasia, analogous to those found in human smokers. The lesions were accompanied by increased expression of proliferating cell nuclear antigen and activation of the serine/threonine kinase Akt in the bronchial epithelium. In contrast, no lung lesions were found in guinea pigs (‘sham smoked’) that were submitted to identical procedures but without cigarettes. Compared with a diet low in vitamin C (50 p.p.m.) and vitamin E (15 p.p.m.), a diet high in vitamin C (4000 p.p.m.) and vitamin E (40 p.p.m.) significantly increased the incidence of these lesions. The inclusion of 1,4-phenylenebis(methylene)selenocyanate (p-XSC), a synthetic chemopreventive organoselenium compound, in the high vitamin C–high vitamin E diet at a level of 15 p.p.m. as selenium appeared to decrease the lesion incidence. Administration of (–)-epigallocatechin gallate, a powerful green tea polyphenolic antioxidant, at 560 p.p.m. in the drinking water had no effect. As in human smokers, levels of ascorbate in blood plasma, lung, liver and the adrenal glands were significantly decreased by cigarette smoke inhalation. These results identify a relevant in vivo laboratory model of cigarette smoke-induced lung cancer, suggest that p-XSC may have activity as a chemopreventive agent against cigarette smoke-induced lung lesions and provide additional evidence that very high dietary levels of certain antioxidants can have co-carcinogenic activity in cigarette smoke-induced lung cancer.
Friday, February 25, 2005
References to Recent Studies on Diet and Cancer
BrooklynDodger received the blogs first posting. No longer a virgin. The post complained about omiting references to recent studies on diet and cancer. The Dodger apologizes, but blames it on editing clumsiness of Blogspot, since the Dodger never makes a mistake. This post conveys the references in JAMA.
Unfortunately, the more interesting reference is the editorial cited below, which has no abstract and is available only in full text. That contains the history of Doll and Peto's canonical assertion that 35% of cancer is due to diet.
The Dodger has chopped the abstracts to the breast and colon cancer studies, which are fully available on medline. The breast cancer and fruit study was very large and very null. The red meat and colon study was null for current consumption, and found an association for high to low long term consumption of red meat.
Although large and powerful, the Dodger suggests these studies must be viewed in context because some unknown artifact in collection of diet data, or unaccounted for social variable in the population [the canonical "uncontrolled confounding"] may account for the results. People who claim the healthy diet may enjoy other aspects of clean living. Therefore, the Dodger gives greater weight to the null study for breast cancer than the association found in the study for nasty red meat.
[For the record, the Dodger pretty much eschews chewing beef at home, although a brat and a beer at the game is a treasured guilty pleasure.]
Thus, this salvo of studies would appear to put "lifestyle" on a diet when weighting causes of variation of rates of cancer in the population.
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JAMA. 2005 Jan 12;293(2):233-4.
Diet and cancer: an evolving picture.Willett WC.Publication Types:
· Comment
· Editorial
JAMA. 2005 Jan 12;293(2):183-93.
Consumption of vegetables and fruits and risk of breast cancer.
van Gils CH, Peeters PH, Bueno-de-Mesquita HB, Boshuizen HC, Lahmann PH, Clavel-Chapelon F, Thiebaut A, Kesse E, Sieri S, Palli D, Tumino R, Panico S, Vineis P, Gonzalez CA, Ardanaz E, Sanchez MJ, Amiano P, Navarro C, Quiros JR, Key TJ, Allen N, Khaw KT, Bingham SA, Psaltopoulou T, Koliva M, Trichopoulou A, Nagel G, Linseisen J, Boeing H, Berglund G, Wirfalt E, Hallmans G, Lenner P, Overvad K, Tjonneland A, Olsen A, Lund E, Engeset D, Alsaker E, Norat T, Kaaks R, Slimani N, Riboli E.Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, The Netherlands.…
Prospective study of 285,526 women between the ages of 25 and 70 years, … No significant associations between vegetable or fruit intake and breast cancer risk were observed. Relative risks for the highest vs the lowest quintile were 0.98 (95% confidence interval [CI], 0.84-1.14) for total vegetables, 1.09 (95% CI , 0.94-1.25) for total fruit, and 1.05 (95% CI , 0.92-1.20) for fruit and vegetable juices. For 6 specific vegetable subgroups no associations with breast cancer risk were observed either. CONCLUSION: Although the period of follow-up is limited for now, the results suggest that total or specific vegetable and fruit intake is not associated with risk for breast cancer.
JAMA. 2005 Jan 12;293(2):172-82.
Meat consumption and risk of colorectal cancer.
Chao A, Thun MJ, Connell CJ, McCullough ML, Jacobs EJ, Flanders WD, Rodriguez C, Sinha R, Calle EE.Epidemiology and Surveillance Research, American Cancer Society, Atlanta, Ga 30329-4251, USA.…
A cohort of 148 610 adults aged 50 to 74 years (median, 63 years), residing in 21 states with population-based cancer registries…High intake of red and processed meat …was associated with higher risk of colon cancer after adjusting for age and energy intake but not after further adjustment for body mass index, cigarette smoking, and other covariates. When long-term consumption was considered, persons in the highest tertile of consumption … had higher risk of distal colon cancer associated with processed meat (RR, 1.50; 95% confidence interval [CI], 1.04-2.17), and ratio of red meat to poultry and fish (RR, 1.53; 95% CI, 1.08-2.18) relative to those persons in the lowest tertile at both time points. Long-term consumption of poultry and fish was inversely associated with risk of both proximal and distal colon cancer. … long-term meat consumption in assessing cancer risk and strengthen the evidence that prolonged high consumption of red and processed meat may increase the risk of cancer in the distal portion of the large intestine
Unfortunately, the more interesting reference is the editorial cited below, which has no abstract and is available only in full text. That contains the history of Doll and Peto's canonical assertion that 35% of cancer is due to diet.
The Dodger has chopped the abstracts to the breast and colon cancer studies, which are fully available on medline. The breast cancer and fruit study was very large and very null. The red meat and colon study was null for current consumption, and found an association for high to low long term consumption of red meat.
Although large and powerful, the Dodger suggests these studies must be viewed in context because some unknown artifact in collection of diet data, or unaccounted for social variable in the population [the canonical "uncontrolled confounding"] may account for the results. People who claim the healthy diet may enjoy other aspects of clean living. Therefore, the Dodger gives greater weight to the null study for breast cancer than the association found in the study for nasty red meat.
[For the record, the Dodger pretty much eschews chewing beef at home, although a brat and a beer at the game is a treasured guilty pleasure.]
Thus, this salvo of studies would appear to put "lifestyle" on a diet when weighting causes of variation of rates of cancer in the population.
VVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVV
JAMA. 2005 Jan 12;293(2):233-4.
Diet and cancer: an evolving picture.Willett WC.Publication Types:
· Comment
· Editorial
JAMA. 2005 Jan 12;293(2):183-93.
Consumption of vegetables and fruits and risk of breast cancer.
van Gils CH, Peeters PH, Bueno-de-Mesquita HB, Boshuizen HC, Lahmann PH, Clavel-Chapelon F, Thiebaut A, Kesse E, Sieri S, Palli D, Tumino R, Panico S, Vineis P, Gonzalez CA, Ardanaz E, Sanchez MJ, Amiano P, Navarro C, Quiros JR, Key TJ, Allen N, Khaw KT, Bingham SA, Psaltopoulou T, Koliva M, Trichopoulou A, Nagel G, Linseisen J, Boeing H, Berglund G, Wirfalt E, Hallmans G, Lenner P, Overvad K, Tjonneland A, Olsen A, Lund E, Engeset D, Alsaker E, Norat T, Kaaks R, Slimani N, Riboli E.Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, The Netherlands.…
Prospective study of 285,526 women between the ages of 25 and 70 years, … No significant associations between vegetable or fruit intake and breast cancer risk were observed. Relative risks for the highest vs the lowest quintile were 0.98 (95% confidence interval [CI], 0.84-1.14) for total vegetables, 1.09 (95% CI , 0.94-1.25) for total fruit, and 1.05 (95% CI , 0.92-1.20) for fruit and vegetable juices. For 6 specific vegetable subgroups no associations with breast cancer risk were observed either. CONCLUSION: Although the period of follow-up is limited for now, the results suggest that total or specific vegetable and fruit intake is not associated with risk for breast cancer.
JAMA. 2005 Jan 12;293(2):172-82.
Meat consumption and risk of colorectal cancer.
Chao A, Thun MJ, Connell CJ, McCullough ML, Jacobs EJ, Flanders WD, Rodriguez C, Sinha R, Calle EE.Epidemiology and Surveillance Research, American Cancer Society, Atlanta, Ga 30329-4251, USA.…
A cohort of 148 610 adults aged 50 to 74 years (median, 63 years), residing in 21 states with population-based cancer registries…High intake of red and processed meat …was associated with higher risk of colon cancer after adjusting for age and energy intake but not after further adjustment for body mass index, cigarette smoking, and other covariates. When long-term consumption was considered, persons in the highest tertile of consumption … had higher risk of distal colon cancer associated with processed meat (RR, 1.50; 95% confidence interval [CI], 1.04-2.17), and ratio of red meat to poultry and fish (RR, 1.53; 95% CI, 1.08-2.18) relative to those persons in the lowest tertile at both time points. Long-term consumption of poultry and fish was inversely associated with risk of both proximal and distal colon cancer. … long-term meat consumption in assessing cancer risk and strengthen the evidence that prolonged high consumption of red and processed meat may increase the risk of cancer in the distal portion of the large intestine
Wednesday, February 23, 2005
Penetrating Particles
BrooklynDodger continues anthologizing particle toxicity. In this report, particles enter circulation within a minute.
Passage of inhaled particles into the blood circulation in humans.
Nemmar A, Hoet PH, Vanquickenborne B, Dinsdale D, Thomeer M, Hoylaerts MF, Vanbilloen H, Mortelmans L, Nemery B.Laboratory of Pneumology (Lung Toxicology, Katholieke Universiteit Leuven, Leuven, Belgium.
BACKGROUND: Pollution by particulates has been consistently associated with increased cardiovascular morbidity and mortality. However, the mechanisms responsible for these effects are not well-elucidated.
METHODS AND RESULTS: To assess to what extent and how rapidly inhaled pollutant particles pass into the systemic circulation, we measured, in 5 healthy volunteers, the distribution of radioactivity after the inhalation of "Technegas," an aerosol consisting mainly of ultrafine (99m)Technetium-labeled carbon particles (<100 nm). Radioactivity was detected in blood already at 1 minute, reached a maximum between 10 and 20 minutes, and remained at this level up to 60 minutes. Thin layer chromatography of blood showed that in addition to a species corresponding to oxidized (99m)Tc, ie, pertechnetate, there was also a species corresponding to particle-bound (99m)Tc. Gamma camera images showed substantial radioactivity over the liver and other areas of the body.
CONCLUSIONS: We conclude that inhaled (99m)Tc-labeled ultrafine carbon particles pass rapidly into the systemic circulation, and this process could account for the well-established, but poorly understood, extrapulmonary effects of air pollution.
Passage of inhaled particles into the blood circulation in humans.
Nemmar A, Hoet PH, Vanquickenborne B, Dinsdale D, Thomeer M, Hoylaerts MF, Vanbilloen H, Mortelmans L, Nemery B.Laboratory of Pneumology (Lung Toxicology, Katholieke Universiteit Leuven, Leuven, Belgium.
BACKGROUND: Pollution by particulates has been consistently associated with increased cardiovascular morbidity and mortality. However, the mechanisms responsible for these effects are not well-elucidated.
METHODS AND RESULTS: To assess to what extent and how rapidly inhaled pollutant particles pass into the systemic circulation, we measured, in 5 healthy volunteers, the distribution of radioactivity after the inhalation of "Technegas," an aerosol consisting mainly of ultrafine (99m)Technetium-labeled carbon particles (<100 nm). Radioactivity was detected in blood already at 1 minute, reached a maximum between 10 and 20 minutes, and remained at this level up to 60 minutes. Thin layer chromatography of blood showed that in addition to a species corresponding to oxidized (99m)Tc, ie, pertechnetate, there was also a species corresponding to particle-bound (99m)Tc. Gamma camera images showed substantial radioactivity over the liver and other areas of the body.
CONCLUSIONS: We conclude that inhaled (99m)Tc-labeled ultrafine carbon particles pass rapidly into the systemic circulation, and this process could account for the well-established, but poorly understood, extrapulmonary effects of air pollution.
Tuesday, February 22, 2005
Particles on the Brain
BrooklynDodger continues with the big story of the 21st century in occupational and environmental health. That story is the lung toxicity of particles without specific toxicity [in contrast to silica and asbestos] and the additional ability of ultrafine particles to penetrate the lungs into the rest of the body.
The burst of work on lung toxicity of "non-toxic" particles began following the observation that inhaled diesel particulate matter was carcinogenic in the rat, about 100 times as potent as cigarette smoke. But, clean carbon particles [carbon black] had potency equivalent to DPM.
The burst of work on penetration of ultra fine particles was prompted by the observation in people of increased cardiac mortality with increased particulate exposure in community studies.
In this study, the investigators found two things at carbon particle exposures very low compared to occupational limits. OSHA permits respirable particle exposures of 5000 micrograms per cubic meter, 8 hours a day for a working lifetime. Exposures in this study were 160 micrograms per cubic meter for 6 hours. EPA permits small particle exposures of 15 micrograms per cubic meter, but increased mortality is observed at these levels.
First, particles persisted in the lungs for a week, and certainly much longer. Second, these particles penetrated the brain, in spite of the blood brain barrier.
The following paraphrases the abstract, followed by the full reference:
We generated ultrafine elemental radioactive carbon particles at a concentration of 160 microg/m(3). Rats were exposed for 6 h. Lung concentration decreased from 1.39 microg/g (day 1) to 0.59 microg/g by 7 days postexposure. [Dodger: initially deposited carbon particles were only ½ cleared out of the lungs in 1 week.] Day 1 (13)C concentrations of cerebrum and cerebellum were also significantly increased but the increase was inconsistent, significant only on one additional day of the postexposure period…. We conclude from our study that the CNS can be targeted by airborne solid ultrafine particles and that the most likely mechanism is from deposits on the olfactory mucosa of the nasopharyngeal region of the respiratory tract and subsequent translocation via the olfactory nerve.
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Inhal Toxicol. 2004 Jun;16(6-7):437-45.
Translocation of inhaled ultrafine particles to the brain.Oberdorster G, Sharp Z, Atudorei V, Elder A, Gelein R, Kreyling W, Cox C.Department of Environmental Medicine, University of Rochester, Rochester, New York 14642, USA.
gunter_oberdorster@urmc.rochester.edu
Ultrafine particles (UFP, particles <100>
Our previous rat studies have shown that UFP can translocate to interstitial sites in the respiratory tract as well as to extrapulmonary organs such as liver within 4 to 24 h postexposure. There were also indications that the olfactory bulb of the brain was targeted. Our objective in this follow-up study, therefore, was to determine whether translocation of inhaled ultrafine solid particles to regions of the brain takes place, hypothesizing that UFP depositing on the olfactory mucosa of the nasal region will translocate along the olfactory nerve into the olfactory bulb. This should result in significant increases in that region on the days following the exposure as opposed to other areas of the central nervous system (CNS). We generated ultrafine elemental (13)C particles (CMD = 36 nm; GSD = 1.66) from [(13)C] graphite rods by electric spark discharge in an argon atmosphere at a concentration of 160 microg/m(3). Rats were exposed for 6 h, and lungs, cerebrum, cerebellum and olfactory bulbs were removed 1, 3, 5, and 7 days after exposure. (13)C concentrations were determined by isotope ratio mass spectroscopy and compared to background (13)C levels of sham-exposed controls (day 0). The background corrected pulmonary (13)C added as ultrafine (13)C particles on day 1 postexposure was 1.34 microg/lung. Lung (13)C concentration decreased from 1.39 microg/g (day 1) to 0.59 microg/g by 7 days postexposure. There was a significant and persistent increase in added (13)C in the olfactory bulb of 0.35 microg/g on day 1, which increased to 0.43 microg/g by day 7. Day 1 (13)C concentrations of cerebrum and cerebellum were also significantly increased but the increase was inconsistent, significant only on one additional day of the postexposure period, possibly reflecting translocation across the blood-brain barrier in certain brain regions. The increases in olfactory bulbs are consistent with earlier studies in nonhuman primates and rodents that demonstrated that intranasally instilled solid UFP translocate along axons of the olfactory nerve into the CNS. We conclude from our study that the CNS can be targeted by airborne solid ultrafine particles and that the most likely mechanism is from deposits on the olfactory mucosa of the nasopharyngeal region of the respiratory tract and subsequent translocation via the olfactory nerve. Depending on particle size, >50% of inhaled UFP can be depositing in the nasopharyngeal region during nasal breathing. Preliminary estimates from the present results show that approximately 20% of the UFP deposited on the olfactory mucosa of the rat can be translocated to the olfactory bulb. Such neuronal translocation constitutes an additional not generally recognized clearance pathway for inhaled solid UFP, whose significance for humans, however, still needs to be established. It could provide a portal of entry into the CNS for solid UFP, circumventing the tight blood-brain barrier. Whether this translocation of inhaled UFP can cause CNS effects needs to be determined in future studies.
The burst of work on lung toxicity of "non-toxic" particles began following the observation that inhaled diesel particulate matter was carcinogenic in the rat, about 100 times as potent as cigarette smoke. But, clean carbon particles [carbon black] had potency equivalent to DPM.
The burst of work on penetration of ultra fine particles was prompted by the observation in people of increased cardiac mortality with increased particulate exposure in community studies.
In this study, the investigators found two things at carbon particle exposures very low compared to occupational limits. OSHA permits respirable particle exposures of 5000 micrograms per cubic meter, 8 hours a day for a working lifetime. Exposures in this study were 160 micrograms per cubic meter for 6 hours. EPA permits small particle exposures of 15 micrograms per cubic meter, but increased mortality is observed at these levels.
First, particles persisted in the lungs for a week, and certainly much longer. Second, these particles penetrated the brain, in spite of the blood brain barrier.
The following paraphrases the abstract, followed by the full reference:
We generated ultrafine elemental radioactive carbon particles at a concentration of 160 microg/m(3). Rats were exposed for 6 h. Lung concentration decreased from 1.39 microg/g (day 1) to 0.59 microg/g by 7 days postexposure. [Dodger: initially deposited carbon particles were only ½ cleared out of the lungs in 1 week.] Day 1 (13)C concentrations of cerebrum and cerebellum were also significantly increased but the increase was inconsistent, significant only on one additional day of the postexposure period…. We conclude from our study that the CNS can be targeted by airborne solid ultrafine particles and that the most likely mechanism is from deposits on the olfactory mucosa of the nasopharyngeal region of the respiratory tract and subsequent translocation via the olfactory nerve.
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Inhal Toxicol. 2004 Jun;16(6-7):437-45.
Translocation of inhaled ultrafine particles to the brain.Oberdorster G, Sharp Z, Atudorei V, Elder A, Gelein R, Kreyling W, Cox C.Department of Environmental Medicine, University of Rochester, Rochester, New York 14642, USA.
gunter_oberdorster@urmc.rochester.edu
Ultrafine particles (UFP, particles <100>
Our previous rat studies have shown that UFP can translocate to interstitial sites in the respiratory tract as well as to extrapulmonary organs such as liver within 4 to 24 h postexposure. There were also indications that the olfactory bulb of the brain was targeted. Our objective in this follow-up study, therefore, was to determine whether translocation of inhaled ultrafine solid particles to regions of the brain takes place, hypothesizing that UFP depositing on the olfactory mucosa of the nasal region will translocate along the olfactory nerve into the olfactory bulb. This should result in significant increases in that region on the days following the exposure as opposed to other areas of the central nervous system (CNS). We generated ultrafine elemental (13)C particles (CMD = 36 nm; GSD = 1.66) from [(13)C] graphite rods by electric spark discharge in an argon atmosphere at a concentration of 160 microg/m(3). Rats were exposed for 6 h, and lungs, cerebrum, cerebellum and olfactory bulbs were removed 1, 3, 5, and 7 days after exposure. (13)C concentrations were determined by isotope ratio mass spectroscopy and compared to background (13)C levels of sham-exposed controls (day 0). The background corrected pulmonary (13)C added as ultrafine (13)C particles on day 1 postexposure was 1.34 microg/lung. Lung (13)C concentration decreased from 1.39 microg/g (day 1) to 0.59 microg/g by 7 days postexposure. There was a significant and persistent increase in added (13)C in the olfactory bulb of 0.35 microg/g on day 1, which increased to 0.43 microg/g by day 7. Day 1 (13)C concentrations of cerebrum and cerebellum were also significantly increased but the increase was inconsistent, significant only on one additional day of the postexposure period, possibly reflecting translocation across the blood-brain barrier in certain brain regions. The increases in olfactory bulbs are consistent with earlier studies in nonhuman primates and rodents that demonstrated that intranasally instilled solid UFP translocate along axons of the olfactory nerve into the CNS. We conclude from our study that the CNS can be targeted by airborne solid ultrafine particles and that the most likely mechanism is from deposits on the olfactory mucosa of the nasopharyngeal region of the respiratory tract and subsequent translocation via the olfactory nerve. Depending on particle size, >50% of inhaled UFP can be depositing in the nasopharyngeal region during nasal breathing. Preliminary estimates from the present results show that approximately 20% of the UFP deposited on the olfactory mucosa of the rat can be translocated to the olfactory bulb. Such neuronal translocation constitutes an additional not generally recognized clearance pathway for inhaled solid UFP, whose significance for humans, however, still needs to be established. It could provide a portal of entry into the CNS for solid UFP, circumventing the tight blood-brain barrier. Whether this translocation of inhaled UFP can cause CNS effects needs to be determined in future studies.
Monday, February 21, 2005
(Don't) Be Still My Heart
BrooklynDodger believes that community studies of the last decade showing increased mortality and illness from cardiovascular causes with increases in particulate exposure present the biggest opportunity in occupational and environmental health.
At the outset, there was limited or no experimental toxicology to support the observation that particles could cause cardiovascular effects. This presented laboratory scientists with a problem equivalent to proving that tobacco smoke could cause cancer. Gradually the problem of replicating health effects in free living humans in the laboratory is being solved.
Key is the recognition that an 0.3 micron particle can penetrate from the lungs into the systemic circulation. Once scientists know it's there, they can devise many studies to measure effects which can't be directly observed in people.
In this study, diesel particulate matter intilled into the lungs affected blood clotting, a key change related to heart disease.
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Toxicol Lett. 2004 Apr 1;149(1-3):243-53.
Possible mechanisms of the cardiovascular effects of inhaled particles: systemic translocation and prothrombotic effects.
Nemmar A, Hoylaerts MF, Hoet PH, Nemery B.Laboratory of Pneumology, Unit of Lung Toxicology, K.U. Leuven, Herestraat, 49, Leuven 3000, Belgium. abderrahim.nemmar@med.kuleuben.ac.be
Particulate air pollution is associated with cardiovascular morbidity and mortality. Fine particles with a diameter <2.5>Recently, we have demonstrated that ultrafine particles are able to translocate from the lung into the systemic circulation in hamsters and humans. In urban areas, diesel engines are considered to be the major source of PM2.5. We therefore evaluated the acute effect (1 h) of diesel exhaust particles (DEP) in a hamster model of peripheral vascular thrombosis induced by free-radical mediated endothelial injury, using intravenous Rose Bengal and local illumination. Intratracheal doses of 5-500 microg of DEP per animal induced inflammation with elevation of neutrophils, total proteins and histamine in bronchoalveolar lavage. DEP enhanced experimental arterial and venous platelet rich-thrombus formation in vivo. Blood samples taken from hamsters 30 and 60 min after instillation of DEP caused platelet activation, when analyzed in the Platelet Function Analyser (PFA-100). The direct addition of DEP to untreated hamster blood also caused platelet aggregation. These effects persisted up to 24 h after instillation. Our results provide plausible mechanistic explanations for the epidemiologically established link between air pollution and acute cardiovascular effects.
At the outset, there was limited or no experimental toxicology to support the observation that particles could cause cardiovascular effects. This presented laboratory scientists with a problem equivalent to proving that tobacco smoke could cause cancer. Gradually the problem of replicating health effects in free living humans in the laboratory is being solved.
Key is the recognition that an 0.3 micron particle can penetrate from the lungs into the systemic circulation. Once scientists know it's there, they can devise many studies to measure effects which can't be directly observed in people.
In this study, diesel particulate matter intilled into the lungs affected blood clotting, a key change related to heart disease.
>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
Toxicol Lett. 2004 Apr 1;149(1-3):243-53.
Possible mechanisms of the cardiovascular effects of inhaled particles: systemic translocation and prothrombotic effects.
Nemmar A, Hoylaerts MF, Hoet PH, Nemery B.Laboratory of Pneumology, Unit of Lung Toxicology, K.U. Leuven, Herestraat, 49, Leuven 3000, Belgium. abderrahim.nemmar@med.kuleuben.ac.be
Particulate air pollution is associated with cardiovascular morbidity and mortality. Fine particles with a diameter <2.5>Recently, we have demonstrated that ultrafine particles are able to translocate from the lung into the systemic circulation in hamsters and humans. In urban areas, diesel engines are considered to be the major source of PM2.5. We therefore evaluated the acute effect (1 h) of diesel exhaust particles (DEP) in a hamster model of peripheral vascular thrombosis induced by free-radical mediated endothelial injury, using intravenous Rose Bengal and local illumination. Intratracheal doses of 5-500 microg of DEP per animal induced inflammation with elevation of neutrophils, total proteins and histamine in bronchoalveolar lavage. DEP enhanced experimental arterial and venous platelet rich-thrombus formation in vivo. Blood samples taken from hamsters 30 and 60 min after instillation of DEP caused platelet activation, when analyzed in the Platelet Function Analyser (PFA-100). The direct addition of DEP to untreated hamster blood also caused platelet aggregation. These effects persisted up to 24 h after instillation. Our results provide plausible mechanistic explanations for the epidemiologically established link between air pollution and acute cardiovascular effects.
Sunday, February 20, 2005
Body Mass Index Hysteria
BrooklynDodger was about to post some extracts on obsesity and health. CDC says that 64% of Americans are overweight or obese, with 30% obsese, so it's now a pretty normal condition. CDC recently retracted an overestimate of the costs of obsesity. A group observed that under this definition, Tom Brady, Kobe Bryant and President Bush are all overweight.
Then the Dodger got sidetracked into wondering who first defined BMI and what it translates into when put in terms of feet and inches. So far, the Dodger has been defeated in attempts to discover the first publication of this index. There are many BMI calculators and tables on the internet, but the Dodger felt that one height and set of weights would illustrate this better.
[The Dodger urges readers not to place any personal significance on the choice of a 6 foot tall person as an example.]
Scientific literature indicates that underweight is associated with poor health outcomes. Too little of anything appears to be bad for you, just like too much. The Dodger would concur that there's something peculiar about a 6 foot tall person weighing less than 136 pounds, although studies indicate that this degree of calorie restriction in laboratory animals prolongs life and reduces cancer. Certainly this weight stratum would be expected to be richer in smokers and poorer in drinkers than higher strata.
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6’ tall
Underweight
BMI = <18.5>Normal weight
BMI = 18.5-24.9
137 – 184 lbs
Overweight
BMI = 25-29.9
184-221 lbs
Obese
BMI = 30 - 35
221 - 258
Then the Dodger got sidetracked into wondering who first defined BMI and what it translates into when put in terms of feet and inches. So far, the Dodger has been defeated in attempts to discover the first publication of this index. There are many BMI calculators and tables on the internet, but the Dodger felt that one height and set of weights would illustrate this better.
[The Dodger urges readers not to place any personal significance on the choice of a 6 foot tall person as an example.]
Scientific literature indicates that underweight is associated with poor health outcomes. Too little of anything appears to be bad for you, just like too much. The Dodger would concur that there's something peculiar about a 6 foot tall person weighing less than 136 pounds, although studies indicate that this degree of calorie restriction in laboratory animals prolongs life and reduces cancer. Certainly this weight stratum would be expected to be richer in smokers and poorer in drinkers than higher strata.
>>>>>>>>>>>>>>>>>>>>>>>>>>
6’ tall
Underweight
BMI = <18.5>Normal weight
BMI = 18.5-24.9
137 – 184 lbs
Overweight
BMI = 25-29.9
184-221 lbs
Obese
BMI = 30 - 35
221 - 258
Friday, February 18, 2005
OSHA Standards and Democracy
The story below springboards an explanation of why the OSHA standard setting hearing is the most democratic government process worldwide. And why NAM missed the point of those hearings entirely.
NAM originally got bent out of shape [in the year 2000] because OSHA engaged a team of leading experts in ergonomics to provide scientific reviews and testimony at the ergonomics hearings.
The democracy of OSHA standards hearings starts with OSHA having to put on its evidence supporting the proposed standard. Most agencies put a written review in the record, and take written comments. OSHA prepares that review [the preamble], but also puts its own staff on the witness stand to be questioned by any of the parties to the hearing, management or labor. On the record, government staff have to answer the questions the parties want answered, not what OSHA wants to answer.
But wait, there’s more.
By practice, OSHA presents at its expense the leading experts in the field, the authors of parts of OSHA’s preamble and frequently the studies on which the preamble was based. Most of these are university faculty who would otherwise be sitting back at their institution doing research or teaching. Some don’t do any expert witnessing because it detracts from their main career. But OSHA brings them to the hearing room to present the parts of their work relevant to the key issues in setting a standard. And, in the case of ergonomics, to sit there and answer snarky questions from management lawyers such as Eugene Scalia. Scalia, son of the Supreme Scalia, was then representing United Parcel Service and Budweiser. Later he was appointed Solicitor of Labor in the first term of the second Bush Administration, although he was never confirmed by the Senate and left office.
So OSHA’s presenting expert witnesses is a service to opponents of the standard. Instead of commenting on a peer reviewed scientific paper, those who disagree [or agree] with the leading scientific experts get to frame their exact questions and get answers on the record. Thus, OSHA had provided a service to the opponents of its rule by bringing these academic fish into the hearing room barrel, to be shot at by management’s lawyers. [Mostly, they missed, the gang that couldn’t shoot straight.]
[The record is what people quote in their later lawsuits or before Congress and the public.]
What goes around, comes around. First, unlike a congressional hearing, any party of interest may present evidence and request air time. At a price. Management, and labor and public health organizations, also have to read their testimony and put their spokespersons on the stand to be questioned by the other side, and by OSHA. Because it’s not a courtroom [where the lawyer can say “I’m asking the questions here”], cross examination in an OSHA hearing can be a full contact sport in which the lawyer gets hit as well.
This OSHA hearing process [and subsequent litigation] work so well to produce standards both protective and feasible, that the whole bad guy effort centers on preventing a proposal from being issued and hearings held.
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January 24, 2005
How Quickly They Forget...
Not sure how many of you are following the recent flap over the Department of Education and Armstrong Williams, the conservative African-American commentator. The press has seized upon this as the scandal of the decade, in that Williams was allegedly [actually, Williams admitted this and apologized] paid to hype the "No Child Left Behind Act" on his radio show. ….
So why is this on a blog dealing with manufacturing issues? Because it was not very long ago when the Clinton Administration's Labor Department -- OSHA, to be precise -- paid over 20 witnesses $10,000 each to come testify in favor of its flimsy ergonomics regulation. I… the money was just doled out to allies ("cronies" has such a pejorative connotation) of the Administration and the rule. We raised a stink at the time Download file(Click here to download letter to OSHA), but the only reporter who found it a little, uh, aromatic was John McCaslin of the Washington Times, who ran a piece on it. …. They're outraged that the US Government would pay people to support their point of view without either of them disclosing it. What's so ironic is that this isn't what the Department of Education did, but it is precisely what OSHA did, to a collective yawn from the press, save one.
How quickly they forget, indeed.
Posted by Pat Cleary, vice president of NAM, at January 24, 2005 09:42 AM
NAM originally got bent out of shape [in the year 2000] because OSHA engaged a team of leading experts in ergonomics to provide scientific reviews and testimony at the ergonomics hearings.
The democracy of OSHA standards hearings starts with OSHA having to put on its evidence supporting the proposed standard. Most agencies put a written review in the record, and take written comments. OSHA prepares that review [the preamble], but also puts its own staff on the witness stand to be questioned by any of the parties to the hearing, management or labor. On the record, government staff have to answer the questions the parties want answered, not what OSHA wants to answer.
But wait, there’s more.
By practice, OSHA presents at its expense the leading experts in the field, the authors of parts of OSHA’s preamble and frequently the studies on which the preamble was based. Most of these are university faculty who would otherwise be sitting back at their institution doing research or teaching. Some don’t do any expert witnessing because it detracts from their main career. But OSHA brings them to the hearing room to present the parts of their work relevant to the key issues in setting a standard. And, in the case of ergonomics, to sit there and answer snarky questions from management lawyers such as Eugene Scalia. Scalia, son of the Supreme Scalia, was then representing United Parcel Service and Budweiser. Later he was appointed Solicitor of Labor in the first term of the second Bush Administration, although he was never confirmed by the Senate and left office.
So OSHA’s presenting expert witnesses is a service to opponents of the standard. Instead of commenting on a peer reviewed scientific paper, those who disagree [or agree] with the leading scientific experts get to frame their exact questions and get answers on the record. Thus, OSHA had provided a service to the opponents of its rule by bringing these academic fish into the hearing room barrel, to be shot at by management’s lawyers. [Mostly, they missed, the gang that couldn’t shoot straight.]
[The record is what people quote in their later lawsuits or before Congress and the public.]
What goes around, comes around. First, unlike a congressional hearing, any party of interest may present evidence and request air time. At a price. Management, and labor and public health organizations, also have to read their testimony and put their spokespersons on the stand to be questioned by the other side, and by OSHA. Because it’s not a courtroom [where the lawyer can say “I’m asking the questions here”], cross examination in an OSHA hearing can be a full contact sport in which the lawyer gets hit as well.
This OSHA hearing process [and subsequent litigation] work so well to produce standards both protective and feasible, that the whole bad guy effort centers on preventing a proposal from being issued and hearings held.
>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
January 24, 2005
How Quickly They Forget...
Not sure how many of you are following the recent flap over the Department of Education and Armstrong Williams, the conservative African-American commentator. The press has seized upon this as the scandal of the decade, in that Williams was allegedly [actually, Williams admitted this and apologized] paid to hype the "No Child Left Behind Act" on his radio show. ….
So why is this on a blog dealing with manufacturing issues? Because it was not very long ago when the Clinton Administration's Labor Department -- OSHA, to be precise -- paid over 20 witnesses $10,000 each to come testify in favor of its flimsy ergonomics regulation. I… the money was just doled out to allies ("cronies" has such a pejorative connotation) of the Administration and the rule. We raised a stink at the time Download file(Click here to download letter to OSHA), but the only reporter who found it a little, uh, aromatic was John McCaslin of the Washington Times, who ran a piece on it. …. They're outraged that the US Government would pay people to support their point of view without either of them disclosing it. What's so ironic is that this isn't what the Department of Education did, but it is precisely what OSHA did, to a collective yawn from the press, save one.
How quickly they forget, indeed.
Posted by Pat Cleary, vice president of NAM, at January 24, 2005 09:42 AM
Wednesday, February 16, 2005
Money Tox - Don't Blow a Gasket
BrooklynDodger considers Regulatory Toxicology and Pharmacology the journal where expert testimony goes to get peer reviewed. The Dodger suspects reviewed by other defense experts. Once it’s peer reviewed, the abstract travels the world like a virus spread by medline, and the full text gets to be considered by IARC and NTP.
This paper has a unique statement of sponsorship: “This study was funded, in part, by a diesel engine manufacturer who has elected not to be identified. The sponsor supplied funds only to conduct the described sampling and laboratory analyses, as part of an ongoing industrial hygiene investigation. The investigation was not conducted in the sponsor’s facility and did not involve their employees.” [If someone figures out there was a risk, the Sponsor, a deep pocket corporation, is still off the hook. Kind of like Novak concealing his source.]
Abstract of abstract with comments:
They measured asbestos fiber release from gaskets during all facets of a complete disassembly and cleaning of a medium duty diesel engine by a "journeyman" mechanic. …Twenty seven of thirty three gaskets contained chrysotile asbestos in concentrations that ranged from 5 to 70%. All but one air monitoring sample reported results below the limit of reliable detection even though plumes of visible dust were evident during various removal, cleaning, and buffing procedures. The detection limit for airborne asbestos fibers in this investigation was influenced by the presence of other shop dust in the air. [Dodger: the other junk in the air coated the filters, thereby hiding the asbestos fibers. “Reliable detection” means ignoring fibers which were there.] Our investigation demonstrates that using shop-standard procedures in an established repair facility, a journeyman mechanic has … exposure to airborne asbestos fibers during disassembly of an engine, approximately 10% or less than that currently considered to be acceptable by OSHA.
BrooklynDodger: Taking into account the non zero zero fiber samples, we expect the TWA exposure to be upwards of 0.01 fibers/cc. Twice, three times, five times? OSHA estimates the risk of cancer at 0.1 fiber/cc to be 7 per thousand, about doubling the population risk of cancer. Being a linear thinker, the Dodger figures the risk of lung cancer from a working career at this job is around 1 per 1000, which is a significant risk.
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Regulatory Toxicology and Pharmacology Volume 41, Issue 2 , March 2005, Pages 113-121
Asbestos exposure from gaskets during disassembly of a medium duty diesel engine
Larry R. Liukonena and Francis W. Weirb, , aTech Con Inc., 5990 Scandia Lane, Burleson, TX 76028, USAbFrancis W. Weir, Ph. D., Inc., 14334 Schroeder Road, Houston, TX 77070, USA Received 28 June 2004. Available online 10 December 2004.
Abstract
Diesel engines have historically used asbestos-containing gaskets leading to concerns of fiber release and mechanic exposure. Other published studies regarding asbestos fiber release during gasket removal have reported on short-duration events; were conducted under simulated work conditions; or had other limitations. There are no comprehensive studies relating to diesel engine gaskets under conditions similar to those reported herein, evaluating asbestos fiber release from gaskets during all facets of a complete disassembly and cleaning of a medium duty diesel engine in a busy repair and service shop by a journeyman mechanic. Asbestos content of all gaskets was identified; all disassembly tasks were described and timed; and personal and area air monitoring was conducted for each task. Twenty seven of thirty three gaskets contained chrysotile asbestos in concentrations that ranged from 5 to 70%. All but one air monitoring sample reported results below the limit of reliable detection even though plumes of visible dust were evident during various removal, cleaning, and buffing procedures. The detection limit for airborne asbestos fibers in this investigation was influenced by the presence of other shop dust in the air. Our investigation demonstrates that using shop-standard procedures in an established repair facility, a journeyman mechanic has very little potential for exposure to airborne asbestos fibers during disassembly of an engine, approximately 10% or less than that currently considered to be acceptable by OSHA.
Keywords: Diesel engine; Asbestos; Gaskets; Mechanics; Workplace exposure; Exposure assessment
The authors each provide independent consultative services to a variety of organizations assisting them in resolving industrial hygiene and/or toxicology related issues. From time to time, as in the project forming the basis for this study, we work jointly. This study was funded, in part, by a diesel engine manufacturer who has elected not to be identified. The sponsor supplied funds only to conduct the described sampling and laboratory analyses, as part of an ongoing industrial hygiene investigation. The investigation was not conducted in the sponsor’s facility and did not involve their employees. The sponsor exerted no influence on the content of a report, nor did they contribute in any manner to the preparation of the manuscript. Since the thrust of the study was to examine a generic procedure with direct application to all similar equipment, the identity of the specific engine used in the study, although well described by type and configuration, is not of importance to the interpretation of the data for the reader. All interpretation of the data and opinions relating to the investigation are those of the authors. Time and costs associated with the interpretation of the data and preparation of the manuscript were funded by the authors.Corresponding author. Fax: +1 832 237 7504
This paper has a unique statement of sponsorship: “This study was funded, in part, by a diesel engine manufacturer who has elected not to be identified. The sponsor supplied funds only to conduct the described sampling and laboratory analyses, as part of an ongoing industrial hygiene investigation. The investigation was not conducted in the sponsor’s facility and did not involve their employees.” [If someone figures out there was a risk, the Sponsor, a deep pocket corporation, is still off the hook. Kind of like Novak concealing his source.]
Abstract of abstract with comments:
They measured asbestos fiber release from gaskets during all facets of a complete disassembly and cleaning of a medium duty diesel engine by a "journeyman" mechanic. …Twenty seven of thirty three gaskets contained chrysotile asbestos in concentrations that ranged from 5 to 70%. All but one air monitoring sample reported results below the limit of reliable detection even though plumes of visible dust were evident during various removal, cleaning, and buffing procedures. The detection limit for airborne asbestos fibers in this investigation was influenced by the presence of other shop dust in the air. [Dodger: the other junk in the air coated the filters, thereby hiding the asbestos fibers. “Reliable detection” means ignoring fibers which were there.] Our investigation demonstrates that using shop-standard procedures in an established repair facility, a journeyman mechanic has … exposure to airborne asbestos fibers during disassembly of an engine, approximately 10% or less than that currently considered to be acceptable by OSHA.
BrooklynDodger: Taking into account the non zero zero fiber samples, we expect the TWA exposure to be upwards of 0.01 fibers/cc. Twice, three times, five times? OSHA estimates the risk of cancer at 0.1 fiber/cc to be 7 per thousand, about doubling the population risk of cancer. Being a linear thinker, the Dodger figures the risk of lung cancer from a working career at this job is around 1 per 1000, which is a significant risk.
>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
Regulatory Toxicology and Pharmacology Volume 41, Issue 2 , March 2005, Pages 113-121
Asbestos exposure from gaskets during disassembly of a medium duty diesel engine
Larry R. Liukonena and Francis W. Weirb, , aTech Con Inc., 5990 Scandia Lane, Burleson, TX 76028, USAbFrancis W. Weir, Ph. D., Inc., 14334 Schroeder Road, Houston, TX 77070, USA Received 28 June 2004. Available online 10 December 2004.
Abstract
Diesel engines have historically used asbestos-containing gaskets leading to concerns of fiber release and mechanic exposure. Other published studies regarding asbestos fiber release during gasket removal have reported on short-duration events; were conducted under simulated work conditions; or had other limitations. There are no comprehensive studies relating to diesel engine gaskets under conditions similar to those reported herein, evaluating asbestos fiber release from gaskets during all facets of a complete disassembly and cleaning of a medium duty diesel engine in a busy repair and service shop by a journeyman mechanic. Asbestos content of all gaskets was identified; all disassembly tasks were described and timed; and personal and area air monitoring was conducted for each task. Twenty seven of thirty three gaskets contained chrysotile asbestos in concentrations that ranged from 5 to 70%. All but one air monitoring sample reported results below the limit of reliable detection even though plumes of visible dust were evident during various removal, cleaning, and buffing procedures. The detection limit for airborne asbestos fibers in this investigation was influenced by the presence of other shop dust in the air. Our investigation demonstrates that using shop-standard procedures in an established repair facility, a journeyman mechanic has very little potential for exposure to airborne asbestos fibers during disassembly of an engine, approximately 10% or less than that currently considered to be acceptable by OSHA.
Keywords: Diesel engine; Asbestos; Gaskets; Mechanics; Workplace exposure; Exposure assessment
The authors each provide independent consultative services to a variety of organizations assisting them in resolving industrial hygiene and/or toxicology related issues. From time to time, as in the project forming the basis for this study, we work jointly. This study was funded, in part, by a diesel engine manufacturer who has elected not to be identified. The sponsor supplied funds only to conduct the described sampling and laboratory analyses, as part of an ongoing industrial hygiene investigation. The investigation was not conducted in the sponsor’s facility and did not involve their employees. The sponsor exerted no influence on the content of a report, nor did they contribute in any manner to the preparation of the manuscript. Since the thrust of the study was to examine a generic procedure with direct application to all similar equipment, the identity of the specific engine used in the study, although well described by type and configuration, is not of importance to the interpretation of the data for the reader. All interpretation of the data and opinions relating to the investigation are those of the authors. Time and costs associated with the interpretation of the data and preparation of the manuscript were funded by the authors.Corresponding author. Fax: +1 832 237 7504
Tuesday, February 15, 2005
Diet Recedes as Cause of Cancer
BrooklynDodger a few years ago attended a public meeting linking cancer to the environment. For virtually every tumor site, “diet” was claimed to be a risk factor, mostly not eating enough vegetables [like your mother told you to] and too much meat [maybe not what your mother said.] Some recent publications undermine some of this blame-the-victimology.
Most of this diet centric view arises from not knowing anything about chemical exposures.
So today BrooklynDodger posts 3 publications.
First, a review of diet and cancer, which outlines the history following the [bogus] Doll and Peto claim that 35% of cancer deaths were attributed to dietary factors. The reviewer concedes that the “too much fat” hypothesis has fallen, and that vegetables don’t prevent breast cancer. A recent study linking red meat and colorectal cancer is cited as showing there is a connection.
The references to these two studies follow.
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Most of this diet centric view arises from not knowing anything about chemical exposures.
So today BrooklynDodger posts 3 publications.
First, a review of diet and cancer, which outlines the history following the [bogus] Doll and Peto claim that 35% of cancer deaths were attributed to dietary factors. The reviewer concedes that the “too much fat” hypothesis has fallen, and that vegetables don’t prevent breast cancer. A recent study linking red meat and colorectal cancer is cited as showing there is a connection.
The references to these two studies follow.
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Sunday, February 13, 2005
Ozone Kills at Levels Permitted by EPA
BrooklynDodger posts yet another study showing that air pollution permitted by current EPA limits – in this case ozone – causes directly observed increases in deaths in community studies. Key comments of the investigators extracted from the full text are:
"A 10-ppb increase in daily ozone would correspond to an additional 319 … annual premature deaths for New York City and 3767 … premature deaths annually for the 95 urban communities, based on mortality data from 2000. This value is probably an underestimate of the total mortality burden from such an increase in ozone because it accounts for only the short-term effects. Further, we found a relationship between mortality and ozone at pollution levels below the current regulatory standard."
The new EPA limit for ozone is 80 ppb; most communities included in this study had exposure below the EPA limit.
So if EPA and the Administration accepted the results, they would conclude that current regulatory approaches allow too much exposure. Compliance with the NAAQS rule for ozone will still leave behind excess deaths. New source performance rules which might administratively require better control are certainly needed.
This study was accepted through peer review by a top ranked US medical journal – Journal of the American Medical Association – and co authored by a leading epidemiologist.
These studies depend on advanced statistical techniques. These techniques have been extensively reviewed and survived concerted attack by industry.
>>>>>>>>>>>>>>>>>>>>>>
Ozone and Short-term Mortality in 95 US Urban Communities, 1987-2000
Michelle L. Bell, PhD; Aidan McDermott, PhD; Scott L. Zeger, PhD; Jonathan M. Samet, MD; Francesca Dominici, PhD
JAMA. 2004;292:2372-2378.
Context Ozone has been associated with various adverse health effects, including increased rates of hospital admissions and exacerbation of respiratory illnesses. Although numerous time-series studies have estimated associations between day-to-day variation in ozone levels and mortality counts, results have been inconclusive.
Objective To investigate whether short-term (daily and weekly) exposure to ambient ozone is associated with mortality in the United States.
Design and Setting Using analytical methods and databases developed for the National Morbidity, Mortality, and Air Pollution Study, we estimated a national average relative rate of mortality associated with short-term exposure to ambient ozone for 95 large US urban communities from 1987-2000. We used distributed-lag models for estimating community-specific relative rates of mortality adjusted for time-varying confounders (particulate matter, weather, seasonality, and long-term trends) and hierarchical models for combining relative rates across communities to estimate a national average relative rate, taking into account spatial heterogeneity.
Main Outcome Measure Daily counts of total non–injury-related mortality and cardiovascular and respiratory mortality in 95 large US communities during a 14-year period.
Results A 10-ppb increase in the previous week’s ozone was associated with a 0.52% increase in daily mortality (95% posterior interval [PI], 0.27%-0.77%) and a 0.64% increase in cardiovascular and respiratory mortality (95% PI, 0.31%-0.98%). Effect estimates for aggregate ozone during the previous week were larger than for models considering only a single day’s exposure. Results were robust to adjustment for particulate matter, weather, seasonality, and long-term trends.
Conclusions These results indicate a statistically significant association between short-term changes in ozone and mortality on average for 95 large US urban communities, which include about 40% of the total US population. The findings indicate that this widespread pollutant adversely affects public health.
"A 10-ppb increase in daily ozone would correspond to an additional 319 … annual premature deaths for New York City and 3767 … premature deaths annually for the 95 urban communities, based on mortality data from 2000. This value is probably an underestimate of the total mortality burden from such an increase in ozone because it accounts for only the short-term effects. Further, we found a relationship between mortality and ozone at pollution levels below the current regulatory standard."
The new EPA limit for ozone is 80 ppb; most communities included in this study had exposure below the EPA limit.
So if EPA and the Administration accepted the results, they would conclude that current regulatory approaches allow too much exposure. Compliance with the NAAQS rule for ozone will still leave behind excess deaths. New source performance rules which might administratively require better control are certainly needed.
This study was accepted through peer review by a top ranked US medical journal – Journal of the American Medical Association – and co authored by a leading epidemiologist.
These studies depend on advanced statistical techniques. These techniques have been extensively reviewed and survived concerted attack by industry.
>>>>>>>>>>>>>>>>>>>>>>
Ozone and Short-term Mortality in 95 US Urban Communities, 1987-2000
Michelle L. Bell, PhD; Aidan McDermott, PhD; Scott L. Zeger, PhD; Jonathan M. Samet, MD; Francesca Dominici, PhD
JAMA. 2004;292:2372-2378.
Context Ozone has been associated with various adverse health effects, including increased rates of hospital admissions and exacerbation of respiratory illnesses. Although numerous time-series studies have estimated associations between day-to-day variation in ozone levels and mortality counts, results have been inconclusive.
Objective To investigate whether short-term (daily and weekly) exposure to ambient ozone is associated with mortality in the United States.
Design and Setting Using analytical methods and databases developed for the National Morbidity, Mortality, and Air Pollution Study, we estimated a national average relative rate of mortality associated with short-term exposure to ambient ozone for 95 large US urban communities from 1987-2000. We used distributed-lag models for estimating community-specific relative rates of mortality adjusted for time-varying confounders (particulate matter, weather, seasonality, and long-term trends) and hierarchical models for combining relative rates across communities to estimate a national average relative rate, taking into account spatial heterogeneity.
Main Outcome Measure Daily counts of total non–injury-related mortality and cardiovascular and respiratory mortality in 95 large US communities during a 14-year period.
Results A 10-ppb increase in the previous week’s ozone was associated with a 0.52% increase in daily mortality (95% posterior interval [PI], 0.27%-0.77%) and a 0.64% increase in cardiovascular and respiratory mortality (95% PI, 0.31%-0.98%). Effect estimates for aggregate ozone during the previous week were larger than for models considering only a single day’s exposure. Results were robust to adjustment for particulate matter, weather, seasonality, and long-term trends.
Conclusions These results indicate a statistically significant association between short-term changes in ozone and mortality on average for 95 large US urban communities, which include about 40% of the total US population. The findings indicate that this widespread pollutant adversely affects public health.
Saturday, February 12, 2005
Marriage Penalty?
BrooklynDodger noted this huge and decidedly peculiar study of 80,000 women in relation to life transitions.
Compared with women who remained married, women who divorced/widowed lost weight. Compared with women who remained unmarried, women who remarried gained weight. Women who divorced increased physical activity compared with women who stayed married. Among non-smokers and past smokers, women who divorced/widowed had more than a twofold increased risk of relapsing/starting smoking than women who stayed married. Divorced and widowed women had decreased vegetable intake relative to women who stayed married.
So BrooklynDodger concludes that women who lose or get rid of their guy start smoking, eat less vegetables, exercise more and lose weight. The Dodger thinks this sounds like going out on the town partying. Definitely “Sex in the City.” There’s literature that smoking helps weight control. The Dodger wonders at the biological plausibility of finding that marriage leads to weight gain.
Another thought. The latest front of the CDC-corporate blame the victim campaign is obesity. BrooklynDodger thinks this is an early salvo aimed at denying health care and health insurance to "guilty victims" of illness, in this case people who are heavy. In this study, marriage [actually remarriage] causes weight gain in women, which moves opposite to the notion of marriage as protective.
>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
International Journal of Epidemiology 2005 34(1):69-78; doi:10.1093/ije/dyh258
Effects of marital transitions on changes in dietary and other health behaviours in US women
Sunmin Lee1,2, Eunyoung Cho1, Francine Grodstein1,3, Ichiro Kawachi1,2,4, Frank B Hu1,5 and Graham A Colditz1,3,6
1 Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA2 Department of Society, Human Development and Health, Harvard School of Public Health, Boston, MA, USA3 Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA4 Harvard Center for Society and Health, Boston, MA, USA5 Department of Nutrition, Harvard School of Public Health, Boston, MA, USA6 Harvard Center for Cancer Prevention, Boston, MA, USA
Correspondence: Sunmin Lee, 33 Pond Avenue, 708, Brookline, MA 02445, USA. E-mail : slee@hsph.harvard.edu
Background Previous studies have indicated that married people have lower mortality and are generally healthier. Most previous studies have been cross-sectional and few studies investigated the effect of marital transition on health. With a prospective design and repeated measures of variables, we sought to analyse the temporal relation between marital transition and change in health behaviours.
Methods We followed up 80 944 women aged 46–71 for 4 years (1992–1996). All information was self-reported. We used multivariate-adjusted linear and logistic regression models to examine the impact of changes in marital status on concomitant changes in health behaviours, controlling for potential confounders and baseline health behaviours.
Results Compared with women who remained married, women who divorced/widowed had body mass index (BMI) decreases of 0.65 kg/m2 (P < 0.001) and 0.44 kg/m2 (P < 0.001), respectively. Compared with women who remained unmarried, women who remarried had an increase in mean BMI of 0.41 kg/m2 (P < 0.001). Women who divorced increased physical activity by 1.23 metabolic equivalent hours (MET)/week (P = 0.07) compared with women who stayed married. Among non-smokers and past smokers, women who divorced/widowed had more than a twofold increased risk of relapsing/starting smoking (OR = 2.47, 95% CI: 1.56, 3.89; OR = 2.08, 95% CI: 1.56, 2.76, respectively) than women who stayed married. Divorced and widowed women had decreased vegetable intake relative to women who stayed married (–2.93 servings/week [P < 0.001] and –1.67 servings/week [P < 0.001], respectively).
Conclusions These patterns suggest both health-damaging and health-promoting changes accompanying divorce and widowhood, and generally health-promoting changes following remarriage.
Compared with women who remained married, women who divorced/widowed lost weight. Compared with women who remained unmarried, women who remarried gained weight. Women who divorced increased physical activity compared with women who stayed married. Among non-smokers and past smokers, women who divorced/widowed had more than a twofold increased risk of relapsing/starting smoking than women who stayed married. Divorced and widowed women had decreased vegetable intake relative to women who stayed married.
So BrooklynDodger concludes that women who lose or get rid of their guy start smoking, eat less vegetables, exercise more and lose weight. The Dodger thinks this sounds like going out on the town partying. Definitely “Sex in the City.” There’s literature that smoking helps weight control. The Dodger wonders at the biological plausibility of finding that marriage leads to weight gain.
Another thought. The latest front of the CDC-corporate blame the victim campaign is obesity. BrooklynDodger thinks this is an early salvo aimed at denying health care and health insurance to "guilty victims" of illness, in this case people who are heavy. In this study, marriage [actually remarriage] causes weight gain in women, which moves opposite to the notion of marriage as protective.
>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
International Journal of Epidemiology 2005 34(1):69-78; doi:10.1093/ije/dyh258
Effects of marital transitions on changes in dietary and other health behaviours in US women
Sunmin Lee1,2, Eunyoung Cho1, Francine Grodstein1,3, Ichiro Kawachi1,2,4, Frank B Hu1,5 and Graham A Colditz1,3,6
1 Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA2 Department of Society, Human Development and Health, Harvard School of Public Health, Boston, MA, USA3 Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA4 Harvard Center for Society and Health, Boston, MA, USA5 Department of Nutrition, Harvard School of Public Health, Boston, MA, USA6 Harvard Center for Cancer Prevention, Boston, MA, USA
Correspondence: Sunmin Lee, 33 Pond Avenue, 708, Brookline, MA 02445, USA. E-mail : slee@hsph.harvard.edu
Background Previous studies have indicated that married people have lower mortality and are generally healthier. Most previous studies have been cross-sectional and few studies investigated the effect of marital transition on health. With a prospective design and repeated measures of variables, we sought to analyse the temporal relation between marital transition and change in health behaviours.
Methods We followed up 80 944 women aged 46–71 for 4 years (1992–1996). All information was self-reported. We used multivariate-adjusted linear and logistic regression models to examine the impact of changes in marital status on concomitant changes in health behaviours, controlling for potential confounders and baseline health behaviours.
Results Compared with women who remained married, women who divorced/widowed had body mass index (BMI) decreases of 0.65 kg/m2 (P < 0.001) and 0.44 kg/m2 (P < 0.001), respectively. Compared with women who remained unmarried, women who remarried had an increase in mean BMI of 0.41 kg/m2 (P < 0.001). Women who divorced increased physical activity by 1.23 metabolic equivalent hours (MET)/week (P = 0.07) compared with women who stayed married. Among non-smokers and past smokers, women who divorced/widowed had more than a twofold increased risk of relapsing/starting smoking (OR = 2.47, 95% CI: 1.56, 3.89; OR = 2.08, 95% CI: 1.56, 2.76, respectively) than women who stayed married. Divorced and widowed women had decreased vegetable intake relative to women who stayed married (–2.93 servings/week [P < 0.001] and –1.67 servings/week [P < 0.001], respectively).
Conclusions These patterns suggest both health-damaging and health-promoting changes accompanying divorce and widowhood, and generally health-promoting changes following remarriage.
Friday, February 11, 2005
Firearms and Youth Death
BrooklynDodger returns to the uncontroversial theme of firearms related injuries. As the Dodger understands it, the gun lobby rationalizes ownership based on protection of family. Other studies show that the largest risk factor for dying of gunshot is having a gun in the house. This study focused on youth.
For this study, case firearms were identified by involvement in an incident in which a child or adolescent younger than 20 years gained access to a firearm and shot himself/herself intentionally or unintentionally or shot another individual unintentionally. Using random-digit dial telephone sampling, control firearms were identified by identification of eligible households with at least 1 firearm and children living or visiting in the home. Of the shootings associated with the case firearms, 81 were suicide attempts (95% fatal) and 25 were unintentional injuries (52% fatal). Guns from case households were less likely to be stored unloaded than control guns, case guns were less likely to be stored locked, stored separately from ammunition, or to have ammunition that was locked than were control guns. These findings were consistent for both handguns and long guns and were also similar for both suicide attempts and unintentional injuries.
So, your goal of having a gun in the house is to repel a home invasion in not facilitated by putting your unloaded gun in one safe and your ammo in a different safe. For protection against invaders, you want a loaded Glock under your pillow, or at least in your nightstand drawer.
Gun Storage Practices and Risk of Youth Suicide and Unintentional Firearm Injuries
David C. Grossman, MD, MPH; Beth A. Mueller, DrPH; Christine Riedy, PhD, MPH; M. Denise Dowd, MD, MPH; Andres Villaveces, MD, PhD; Janice Prodzinski, BA; Jon Nakagawara, MHA; John Howard, MD; Norman Thiersch, MD; Richard Harruff, MD
JAMA. 2005;293:707-714.
ABSTRACT
Context Household firearms are associated with an elevated risk of firearm death to occupants in the home. Many organizations and health authorities advocate locking firearms and ammunition to prevent access to guns by children and adolescents. The association of these firearm storage practices with the reduction of firearm injury risk is unclear.
Objective To measure the association of specific household firearm storage practices (locking guns, locking ammunition, keeping guns unloaded) and the risk of unintentional and self-inflicted firearm injuries.
Design and Setting Case-control study of firearms in events identified by medical examiner and coroner offices from 37 counties in Washington, Oregon, and Missouri, and 5 trauma centers in Seattle, Spokane, and Tacoma, Wash, and Kansas City, Mo.
Cases and Controls Case firearms were identified by involvement in an incident in which a child or adolescent younger than 20 years gained access to a firearm and shot himself/herself intentionally or unintentionally or shot another individual unintentionally. Firearm assaults and homicides were excluded. We used records from hospitals and medical examiners to ascertain these incidents. Using random-digit dial telephone sampling, control firearms were identified by identification of eligible households with at least 1 firearm and children living or visiting in the home. Controls were frequency matched by age group and county.
Main Exposure Measures The key exposures of interest in this study were: (1) whether the subject firearm was stored in a locked location or with an extrinsic lock; (2) whether the firearm was stored unloaded; (3) whether the firearm was stored both unloaded in a locked location; (4) whether the ammunition for the firearm was stored separately; and (5) whether the ammunition was stored in a locked location. Data regarding the storage status of case and control guns were collected by interview with respondents from the households of case and control firearms.
Results We interviewed 106 respondents with case firearms and 480 with control firearms. Of the shootings associated with the case firearms, 81 were suicide attempts (95% fatal) and 25 were unintentional injuries (52% fatal). After adjustment for potentially confounding variables, guns from case households were less likely to be stored unloaded than control guns (odds ratio [OR], 0.30; 95% confidence interval [CI], 0.16-0.56). Similarly, case guns were less likely to be stored locked (OR, 0.27; 95% CI, 0.17-0.45), stored separately from ammunition (OR, 0.45; 95% CI, 0.34-0.93), or to have ammunition that was locked (OR, 0.39; 95% CI, 0.23-0.66) than were control guns. These findings were consistent for both handguns and long guns and were also similar for both suicide attempts and unintentional injuries.
Conclusions The 4 practices of keeping a gun locked, unloaded, storing ammunition locked, and in a separate location are each associated with a protective effect and suggest a feasible strategy to reduce these types of injuries in homes with children and teenagers where guns are stored.
For this study, case firearms were identified by involvement in an incident in which a child or adolescent younger than 20 years gained access to a firearm and shot himself/herself intentionally or unintentionally or shot another individual unintentionally. Using random-digit dial telephone sampling, control firearms were identified by identification of eligible households with at least 1 firearm and children living or visiting in the home. Of the shootings associated with the case firearms, 81 were suicide attempts (95% fatal) and 25 were unintentional injuries (52% fatal). Guns from case households were less likely to be stored unloaded than control guns, case guns were less likely to be stored locked, stored separately from ammunition, or to have ammunition that was locked than were control guns. These findings were consistent for both handguns and long guns and were also similar for both suicide attempts and unintentional injuries.
So, your goal of having a gun in the house is to repel a home invasion in not facilitated by putting your unloaded gun in one safe and your ammo in a different safe. For protection against invaders, you want a loaded Glock under your pillow, or at least in your nightstand drawer.
Gun Storage Practices and Risk of Youth Suicide and Unintentional Firearm Injuries
David C. Grossman, MD, MPH; Beth A. Mueller, DrPH; Christine Riedy, PhD, MPH; M. Denise Dowd, MD, MPH; Andres Villaveces, MD, PhD; Janice Prodzinski, BA; Jon Nakagawara, MHA; John Howard, MD; Norman Thiersch, MD; Richard Harruff, MD
JAMA. 2005;293:707-714.
ABSTRACT
Context Household firearms are associated with an elevated risk of firearm death to occupants in the home. Many organizations and health authorities advocate locking firearms and ammunition to prevent access to guns by children and adolescents. The association of these firearm storage practices with the reduction of firearm injury risk is unclear.
Objective To measure the association of specific household firearm storage practices (locking guns, locking ammunition, keeping guns unloaded) and the risk of unintentional and self-inflicted firearm injuries.
Design and Setting Case-control study of firearms in events identified by medical examiner and coroner offices from 37 counties in Washington, Oregon, and Missouri, and 5 trauma centers in Seattle, Spokane, and Tacoma, Wash, and Kansas City, Mo.
Cases and Controls Case firearms were identified by involvement in an incident in which a child or adolescent younger than 20 years gained access to a firearm and shot himself/herself intentionally or unintentionally or shot another individual unintentionally. Firearm assaults and homicides were excluded. We used records from hospitals and medical examiners to ascertain these incidents. Using random-digit dial telephone sampling, control firearms were identified by identification of eligible households with at least 1 firearm and children living or visiting in the home. Controls were frequency matched by age group and county.
Main Exposure Measures The key exposures of interest in this study were: (1) whether the subject firearm was stored in a locked location or with an extrinsic lock; (2) whether the firearm was stored unloaded; (3) whether the firearm was stored both unloaded in a locked location; (4) whether the ammunition for the firearm was stored separately; and (5) whether the ammunition was stored in a locked location. Data regarding the storage status of case and control guns were collected by interview with respondents from the households of case and control firearms.
Results We interviewed 106 respondents with case firearms and 480 with control firearms. Of the shootings associated with the case firearms, 81 were suicide attempts (95% fatal) and 25 were unintentional injuries (52% fatal). After adjustment for potentially confounding variables, guns from case households were less likely to be stored unloaded than control guns (odds ratio [OR], 0.30; 95% confidence interval [CI], 0.16-0.56). Similarly, case guns were less likely to be stored locked (OR, 0.27; 95% CI, 0.17-0.45), stored separately from ammunition (OR, 0.45; 95% CI, 0.34-0.93), or to have ammunition that was locked (OR, 0.39; 95% CI, 0.23-0.66) than were control guns. These findings were consistent for both handguns and long guns and were also similar for both suicide attempts and unintentional injuries.
Conclusions The 4 practices of keeping a gun locked, unloaded, storing ammunition locked, and in a separate location are each associated with a protective effect and suggest a feasible strategy to reduce these types of injuries in homes with children and teenagers where guns are stored.
Wednesday, February 09, 2005
Six Days On The Road
“I got a ten forward gears and a Georgia overdrive
I take little white pills and my eyes are open wide
I just passed a "Gimmy" and a "White"
I've been smokin' everything in sight
Six days on the road and now I'm gonna make it home tonight”
Six Days on the Road, Recorded by Dave Dudley
Around New Years 2004, two events of safety significance came together. David Darwin Pedruska, better known as Dave Dudley, who made “Six Days on the Road” a trendsetter in truckers’ music, passed away. “Six Days” came back on the air. And, new Hours of Service rules of the Federal Motor Carrier Safety Administration went into effect with some public attention on January 4, 2004. Injury control professionals should consider the implications of these rules off the highway.
Later in the year, a Court of Appeals overturned the new rules, citing a lack of rationale for less than full protection. No one knows what the rules really are now, but the principles remain.
The new FMCSA rules limited truck drivers to 11 hours driving in a 24 hour cycle. More important, driving must cease 14 hours after going on duty, regardless of time behind the wheel. The driver may continue on duty with non-driving tasks. Driving may resume only after 10 hours off duty. Driving must also stop after 60 hours on duty in 7 consecutive days, or 70 hours in 8 days, to start again only after 34 hours off duty.
The clear rationale is that extended duty beyond 14 hours on a single day, and an average of 8.5 hours a day over a calendar week, are sufficient to impair driving performance to the point of creating an injury hazard to the driver and to others. The FMCSA estimates that the rule will cost the public approximately $3.4 billion over 10 years. The agency estimates that the 10-year discounted monetary value of the benefits (fatalities and injuries prevented, property damage savings) is $6.8 billion.
No one would plausibly argue that such a regulation could be implemented, in the Bush Administration no less, if only the drivers were perceived at risk: it is public fear of being squashed by an 18-wheeler which drove this regulation. Despite the positive cost benefit analysis presented by FMCSA, the trucking industry hates this regulation, suggesting it’s cheaper to pay the insurance premiums than make the schedule changes to prevent the injuries. Current drivers fear loss of income from these rules, even though the cost is increased wages for the additional drivers which would be hired to meet these requirements.
These rules apply to people driving a 10,000 lb vehicle over the road. What do they mean for the industrial setting?
Traffic safety analogies come up all the time in discussion of safety culture and philosophy: violating the speed limit, substance impaired driving, compliance with seatbelt usage. For fixed worksite occupational injury control programs, these analogies are distracting.
First, the potential success of any injury control strategy that depends primarily on attention state, reaction time, judgment, motivation, obedience and dexterity is distinctly limited. All workers perform below their median over a hundred days a year, and perform at their lowest 1% on at least 2 days. Given the certain human error at these rates, such a strategy accepts some finite rate of injury in a fixed environment. If one incident is inevitable, why aren’t two acceptable? Yet this is the situation behind the wheel, if the environment is considered fixed.
Secondly, on the highway, we perceive considerable risk to come from second party drivers and unknown environment dangers which can’t be overcome by first party performance.
Finally, culture supports violations of the injury prevention rules. Speeding, and running red lights, can be eliminated nearly 100% by installing camera systems at strategic locations. [This would also catch a large fraction of the impaired driving behavior which causes injury, without the intrusion in privacy of sobriety checkpoints, and minimize the DWB aspect of increased police traffic enforcement.] Even though public authorities would initially make large amounts of money on this equipment, it is rarely installed because the culture which glorifies speeding and evasion of enforcement resists such installations. Finally, most discussions of traffic safety ignore the remarkable unbroken trend of reduction of fatalities per vehicle mile since the 1920’s, when these statistics were started. This trend applies to one car, two car and pedestrian fatalities. These improvements, continued over so long a time, more likely arise from limited access highways, improved traffic signals, better controlled vehicles and better crash survivability than from changes in driving behavior.
.
Returning to the occupational environment, what are the implications of the assumed the 14 hour day, 60 hour week performance decrement? Obviously, enforcing such a regimen on powered industrial vehicle drivers, skilled trades workers, utility maintenance workers, traveling salesmen and others would have major economic impact under current conditions. Mostly, it would require hiring more workers who would do less overtime.
The scientific question is whether over-the-road truck driving by a professional driver is more subject to performance decrement-induced injury than other tasks. Issues to be evaluated are impact of prolonged static posture and visual surveillance on performance, the control characteristics of the vehicle, falling asleep and pressure to drive at night and in bad weather conditions. These are independent of hours of service.
In the manufacturing environment, second party initiated injuries are rare, other than those associated with PIV’s. Although studies are lacking, it would appear that the driving environment for a PIV is less controlled and more incident prone than driving over the road. PIV collision injuries are best prevented by improving the driving environment, but it appears unlikely that this environment will ever be as collision risk protected as the freeway. Fatigue impaired driver performance within this environment would appear to be subject to similar analysis as the FMCSA rule.
Injury control for skilled trades activities will be most effective by concentrating on identifying guarding opportunities for equipment servicing tasks, fall prevention guarding opportunities, structured hazard identification for high risk tasks leading to environment modification and objectively measurable procedural change. A significant fraction of skilled trades incidents involve powered industrial vehicles, used under more risky conditions than standard PIV operations.
Nevertheless, 80-hour weeks for skilled trades workers are common. Seven day weeks, which eliminate the 34 hour rest period to restart the clock are frequent. Ending at midnight Saturday would mean not starting until 10 am on Monday.
I take little white pills and my eyes are open wide
I just passed a "Gimmy" and a "White"
I've been smokin' everything in sight
Six days on the road and now I'm gonna make it home tonight”
Six Days on the Road, Recorded by Dave Dudley
Around New Years 2004, two events of safety significance came together. David Darwin Pedruska, better known as Dave Dudley, who made “Six Days on the Road” a trendsetter in truckers’ music, passed away. “Six Days” came back on the air. And, new Hours of Service rules of the Federal Motor Carrier Safety Administration went into effect with some public attention on January 4, 2004. Injury control professionals should consider the implications of these rules off the highway.
Later in the year, a Court of Appeals overturned the new rules, citing a lack of rationale for less than full protection. No one knows what the rules really are now, but the principles remain.
The new FMCSA rules limited truck drivers to 11 hours driving in a 24 hour cycle. More important, driving must cease 14 hours after going on duty, regardless of time behind the wheel. The driver may continue on duty with non-driving tasks. Driving may resume only after 10 hours off duty. Driving must also stop after 60 hours on duty in 7 consecutive days, or 70 hours in 8 days, to start again only after 34 hours off duty.
The clear rationale is that extended duty beyond 14 hours on a single day, and an average of 8.5 hours a day over a calendar week, are sufficient to impair driving performance to the point of creating an injury hazard to the driver and to others. The FMCSA estimates that the rule will cost the public approximately $3.4 billion over 10 years. The agency estimates that the 10-year discounted monetary value of the benefits (fatalities and injuries prevented, property damage savings) is $6.8 billion.
No one would plausibly argue that such a regulation could be implemented, in the Bush Administration no less, if only the drivers were perceived at risk: it is public fear of being squashed by an 18-wheeler which drove this regulation. Despite the positive cost benefit analysis presented by FMCSA, the trucking industry hates this regulation, suggesting it’s cheaper to pay the insurance premiums than make the schedule changes to prevent the injuries. Current drivers fear loss of income from these rules, even though the cost is increased wages for the additional drivers which would be hired to meet these requirements.
These rules apply to people driving a 10,000 lb vehicle over the road. What do they mean for the industrial setting?
Traffic safety analogies come up all the time in discussion of safety culture and philosophy: violating the speed limit, substance impaired driving, compliance with seatbelt usage. For fixed worksite occupational injury control programs, these analogies are distracting.
First, the potential success of any injury control strategy that depends primarily on attention state, reaction time, judgment, motivation, obedience and dexterity is distinctly limited. All workers perform below their median over a hundred days a year, and perform at their lowest 1% on at least 2 days. Given the certain human error at these rates, such a strategy accepts some finite rate of injury in a fixed environment. If one incident is inevitable, why aren’t two acceptable? Yet this is the situation behind the wheel, if the environment is considered fixed.
Secondly, on the highway, we perceive considerable risk to come from second party drivers and unknown environment dangers which can’t be overcome by first party performance.
Finally, culture supports violations of the injury prevention rules. Speeding, and running red lights, can be eliminated nearly 100% by installing camera systems at strategic locations. [This would also catch a large fraction of the impaired driving behavior which causes injury, without the intrusion in privacy of sobriety checkpoints, and minimize the DWB aspect of increased police traffic enforcement.] Even though public authorities would initially make large amounts of money on this equipment, it is rarely installed because the culture which glorifies speeding and evasion of enforcement resists such installations. Finally, most discussions of traffic safety ignore the remarkable unbroken trend of reduction of fatalities per vehicle mile since the 1920’s, when these statistics were started. This trend applies to one car, two car and pedestrian fatalities. These improvements, continued over so long a time, more likely arise from limited access highways, improved traffic signals, better controlled vehicles and better crash survivability than from changes in driving behavior.
.
Returning to the occupational environment, what are the implications of the assumed the 14 hour day, 60 hour week performance decrement? Obviously, enforcing such a regimen on powered industrial vehicle drivers, skilled trades workers, utility maintenance workers, traveling salesmen and others would have major economic impact under current conditions. Mostly, it would require hiring more workers who would do less overtime.
The scientific question is whether over-the-road truck driving by a professional driver is more subject to performance decrement-induced injury than other tasks. Issues to be evaluated are impact of prolonged static posture and visual surveillance on performance, the control characteristics of the vehicle, falling asleep and pressure to drive at night and in bad weather conditions. These are independent of hours of service.
In the manufacturing environment, second party initiated injuries are rare, other than those associated with PIV’s. Although studies are lacking, it would appear that the driving environment for a PIV is less controlled and more incident prone than driving over the road. PIV collision injuries are best prevented by improving the driving environment, but it appears unlikely that this environment will ever be as collision risk protected as the freeway. Fatigue impaired driver performance within this environment would appear to be subject to similar analysis as the FMCSA rule.
Injury control for skilled trades activities will be most effective by concentrating on identifying guarding opportunities for equipment servicing tasks, fall prevention guarding opportunities, structured hazard identification for high risk tasks leading to environment modification and objectively measurable procedural change. A significant fraction of skilled trades incidents involve powered industrial vehicles, used under more risky conditions than standard PIV operations.
Nevertheless, 80-hour weeks for skilled trades workers are common. Seven day weeks, which eliminate the 34 hour rest period to restart the clock are frequent. Ending at midnight Saturday would mean not starting until 10 am on Monday.
Saturday, February 05, 2005
Costs and Benefits Over the Road
BrooklynDodger continues to investigate off-the-job safety, taking to heart the National Safety Council’s implication that it is safer to work in an auto factory than to drive one of the cars made therein. NIOSH and OSHA have also announced intentions to devote resources – necessarily diverted from real on the job safety and health – to alliances with employers around employee driving. Behavior is a very low level of control. It's important to understand the higher level of controls, engineering controls.
NHTSA’s recently published report informs this investigation. The comments below will reserve BrooklynDodger’s thinking about contrasts between on-the-job safety and health approaches and over-gthe-road. In addition, BrooklynDodger continues to hate cost benefit analysis, of which cost per life saved analysis depicted here is a variant. Once in a while, someone else figuring out the costs may have some value.
The most interesting part of the report is the list of engineering controls installed in vehicles which contribute to the prevention of death and injury.
Comments.
1. NHTSA has adopted a $3,000,000 per life saved risk management policy. Where did that come from? Presumably, a change won’t be ordered if the lives saved are less.
2. By these methods, in 2002, the payment per life saved was $544,000.
3. The 3 million and 500 thousand become a price points for talking about other public health interventions in other arenas.
4. The cost of safety devices per vehicle was in the range of $800. About 20,000 lives were saved, compared to about 32,000 lives not saved.
5. These devices mainly protect the person purchasing the vehicle, and that person’s passengers. The buyer who is forced to buy self-protection but might have volunteered at some price benefits from the economies for scale requiring everyone to buy the same equipment. BrooklynDodger figures the lower cost is somehow a benefit of regulation.
6. BrooklynDodger wants to know how many jobs were created by the fabrication and installation of the $800 worth of stuff.
>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
NHTSA Report Number DOT HS 809 835 December 2004
Cost Per Life Saved By The Federal Motor Vehicle Safety Standards
Charles J. Kahane, Ph.D. The complete report is available here in pdf format.
Two reports summarize the benefits and costs of the Federal Motor Vehicle Safety Standards (FMVSS). The first report estimates that the FMVSS and other safety technologies saved 328,551 lives in calendar years 1960-2002, including 24,561 in 2002. The second report estimates that the FMVSS added $839 (in 2002 Dollars) to the cost of a car in model year 2001 and $711 to the cost of an LTV.
During calendar year 2002, the core FMVSS saved 20,851 lives, some in these model year 2002 vehicles, but most in earlier vehicles already on the road before 2002. Thus, in 2002 the payment per life saved was $544,000.
The core group of technologies cost an estimated $544,000 (in 2002 Dollars) per life saved in 2002. These numbers indicate the FMVSS are, on the whole, highly cost-effective, far below the $3,000,000 per life saved that the Department of Transportation considers acceptable.
Safety improvements with costs not included are:
Improvements to mid- and lower instrument panels that were never actually required by FMVSS 201.
Voluntary improvements to belts and other systems that improved performance on the frontal NCAP test.
Structural improvements in 2-door cars that reduced TTI(d) in side impact tests, on a voluntary basis, well before the dynamic test was added to FMVSS 214.:
High-penetration resistant (HPR) windshields, on all vehicles by 1966, subsequently incorporated into FMVSS 205.
Improvements to door locks, generally completed well before 1968, subsequently regulated by FMVSS 206.
Front disc brakes, a technology related to FMVSS 105.
Adhesive windshield bonding, a technology related to FMVSS 212.
Conspicuity tape for heavy trailers (FMVSS 108): car and LTV occupants benefit from not hitting the trailers, but the cost accrues on the trailers.
Child safety seats (FMVSS 213): they must be purchased separately and are not part of the cost of a new car or LTV.
The dynamic side-impact test requirement of FMVSS 214: cost studies have been completed, but the estimation of benefits is still underway.
3-point belts for rear-center occupants: benefits are included in the lives-saved report, but cost has not yet been estimated.
The “core” group of safety technologies with costs included:
Dual master cylinders (FMVSS 105)
Energy-absorbing steering assemblies (FMVSS 203/204)
Every type of safety belt at any seat position (FMVSS 208), except 3-point belts for rear-center occupants. Although it is true that lap belts were widely introduced before 1968, much of the impetus came from State laws or regulations. These State laws may be considered Government actions that are “predecessors” of the FMVSS. (But only the costs and benefits from 1968 onward will be included in the core group.) Of course, the FMVSS have played a direct role in many of the improvements to belt systems after 1968 that increased their effectiveness, use and consumer acceptance.
Frontal air bags (FMVSS 208) and on-off switches for passenger air bags in pickup trucks.
Side door beams, regulated by the static test requirement of FMVSS 214.
Roof crush strength, passenger cars (FMVSS 216).
Side marker lamps (FMVSS 108)
Center High Mounted Stop Lamps (FMVSS 108)
Head restraints (FMVSS 202)
Fuel system integrity (FMVSS 301)
Seat back locks in 2-door passenger cars (FMVSS 207)
Windshield washers, and upgraded wipers, for LTVs (FMVSS 104)
Safety devices for power windows (FMVSS 118)
Accelerator-pedal return systems (FMVSS 124)
Seatback padding to provide head impact protection for rear-seat occupants (FMVSS 201)
NHTSA’s recently published report informs this investigation. The comments below will reserve BrooklynDodger’s thinking about contrasts between on-the-job safety and health approaches and over-gthe-road. In addition, BrooklynDodger continues to hate cost benefit analysis, of which cost per life saved analysis depicted here is a variant. Once in a while, someone else figuring out the costs may have some value.
The most interesting part of the report is the list of engineering controls installed in vehicles which contribute to the prevention of death and injury.
Comments.
1. NHTSA has adopted a $3,000,000 per life saved risk management policy. Where did that come from? Presumably, a change won’t be ordered if the lives saved are less.
2. By these methods, in 2002, the payment per life saved was $544,000.
3. The 3 million and 500 thousand become a price points for talking about other public health interventions in other arenas.
4. The cost of safety devices per vehicle was in the range of $800. About 20,000 lives were saved, compared to about 32,000 lives not saved.
5. These devices mainly protect the person purchasing the vehicle, and that person’s passengers. The buyer who is forced to buy self-protection but might have volunteered at some price benefits from the economies for scale requiring everyone to buy the same equipment. BrooklynDodger figures the lower cost is somehow a benefit of regulation.
6. BrooklynDodger wants to know how many jobs were created by the fabrication and installation of the $800 worth of stuff.
>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
NHTSA Report Number DOT HS 809 835 December 2004
Cost Per Life Saved By The Federal Motor Vehicle Safety Standards
Charles J. Kahane, Ph.D. The complete report is available here in pdf format.
Two reports summarize the benefits and costs of the Federal Motor Vehicle Safety Standards (FMVSS). The first report estimates that the FMVSS and other safety technologies saved 328,551 lives in calendar years 1960-2002, including 24,561 in 2002. The second report estimates that the FMVSS added $839 (in 2002 Dollars) to the cost of a car in model year 2001 and $711 to the cost of an LTV.
During calendar year 2002, the core FMVSS saved 20,851 lives, some in these model year 2002 vehicles, but most in earlier vehicles already on the road before 2002. Thus, in 2002 the payment per life saved was $544,000.
The core group of technologies cost an estimated $544,000 (in 2002 Dollars) per life saved in 2002. These numbers indicate the FMVSS are, on the whole, highly cost-effective, far below the $3,000,000 per life saved that the Department of Transportation considers acceptable.
Safety improvements with costs not included are:
Improvements to mid- and lower instrument panels that were never actually required by FMVSS 201.
Voluntary improvements to belts and other systems that improved performance on the frontal NCAP test.
Structural improvements in 2-door cars that reduced TTI(d) in side impact tests, on a voluntary basis, well before the dynamic test was added to FMVSS 214.:
High-penetration resistant (HPR) windshields, on all vehicles by 1966, subsequently incorporated into FMVSS 205.
Improvements to door locks, generally completed well before 1968, subsequently regulated by FMVSS 206.
Front disc brakes, a technology related to FMVSS 105.
Adhesive windshield bonding, a technology related to FMVSS 212.
Conspicuity tape for heavy trailers (FMVSS 108): car and LTV occupants benefit from not hitting the trailers, but the cost accrues on the trailers.
Child safety seats (FMVSS 213): they must be purchased separately and are not part of the cost of a new car or LTV.
The dynamic side-impact test requirement of FMVSS 214: cost studies have been completed, but the estimation of benefits is still underway.
3-point belts for rear-center occupants: benefits are included in the lives-saved report, but cost has not yet been estimated.
The “core” group of safety technologies with costs included:
Dual master cylinders (FMVSS 105)
Energy-absorbing steering assemblies (FMVSS 203/204)
Every type of safety belt at any seat position (FMVSS 208), except 3-point belts for rear-center occupants. Although it is true that lap belts were widely introduced before 1968, much of the impetus came from State laws or regulations. These State laws may be considered Government actions that are “predecessors” of the FMVSS. (But only the costs and benefits from 1968 onward will be included in the core group.) Of course, the FMVSS have played a direct role in many of the improvements to belt systems after 1968 that increased their effectiveness, use and consumer acceptance.
Frontal air bags (FMVSS 208) and on-off switches for passenger air bags in pickup trucks.
Side door beams, regulated by the static test requirement of FMVSS 214.
Roof crush strength, passenger cars (FMVSS 216).
Side marker lamps (FMVSS 108)
Center High Mounted Stop Lamps (FMVSS 108)
Head restraints (FMVSS 202)
Fuel system integrity (FMVSS 301)
Seat back locks in 2-door passenger cars (FMVSS 207)
Windshield washers, and upgraded wipers, for LTVs (FMVSS 104)
Safety devices for power windows (FMVSS 118)
Accelerator-pedal return systems (FMVSS 124)
Seatback padding to provide head impact protection for rear-seat occupants (FMVSS 201)
Friday, February 04, 2005
Ergonomic Study Shows Homework is Hazardous to Health
Applied Ergonomics Volume 36, Issue 2 , March 2005, Pages 193-198
Schoolbag weight and musculoskeletal symptoms in New Zealand secondary schools
J. Whittfield, S.J. Legg , and D.I. Hedderley
Centre for Ergonomics, Occupational Safety and Health, Department of Human Resource Management, College of Business, Massey University, Private Bag 1122, Palmerston North, New Zealand
The weight of schoolbags and the prevalence of musculoskeletal symptoms amongst 140 students (70 third form students comprising 35 females and 35 males, and 70 sixth form students comprising 35 females and 35 males) from five New Zealand secondary schools was investigated. Schoolbag weight for third form students (mean age 13.6 years) was 13.2% of their body weight, while for sixth form students (mean age 17.1 years) it was 10.3% of their body weight. These weights may exceed the recommended guideline load limits for adult industrial workers. Musculoskeletal symptoms were reported by 77.1% of the students. Symptoms were most prevalent in the neck, shoulders, upper back and lower back. Although musculoskeletal symptoms are believed to be multifactorial in origin, the carriage of heavy schoolbags is a suspected contributory factor and may represent an overlooked daily physical stress for New Zealand secondary school students.
Schoolbag weight and musculoskeletal symptoms in New Zealand secondary schools
J. Whittfield, S.J. Legg , and D.I. Hedderley
Centre for Ergonomics, Occupational Safety and Health, Department of Human Resource Management, College of Business, Massey University, Private Bag 1122, Palmerston North, New Zealand
The weight of schoolbags and the prevalence of musculoskeletal symptoms amongst 140 students (70 third form students comprising 35 females and 35 males, and 70 sixth form students comprising 35 females and 35 males) from five New Zealand secondary schools was investigated. Schoolbag weight for third form students (mean age 13.6 years) was 13.2% of their body weight, while for sixth form students (mean age 17.1 years) it was 10.3% of their body weight. These weights may exceed the recommended guideline load limits for adult industrial workers. Musculoskeletal symptoms were reported by 77.1% of the students. Symptoms were most prevalent in the neck, shoulders, upper back and lower back. Although musculoskeletal symptoms are believed to be multifactorial in origin, the carriage of heavy schoolbags is a suspected contributory factor and may represent an overlooked daily physical stress for New Zealand secondary school students.
Thursday, February 03, 2005
Asbestosis and Silicosis, Legislative Update
BrooklynDodger noticed the following in the 1/31 Daily Labor Reporter posting:
Specter Suggests Limiting State Silica Suits to Prevent Dual Filings
"Reacting to new testimony that asbestos- and silica-related disease are easy to distinguish, Senate Judiciary Committee Chairman Specter (R-Pa.) says lawmakers should now be able to draft language in a multibillion-dollar asbestos trust fund bill to prevent asbestos claimants from recasting their claims to refer to other harmful substances, such as silica. "There is no confusing asbestos and silica-related disease," Specter says after a hearing on the issue of "mixed dust" claims. "That should leave us a clear path to eliminate second claims" of asbestos claimants in court. "
>>>>>>>>>>>>>>>>>>>>>>>>>>>>
BrooklynDodger is not going to take a position here on asbestos compensation legislation or Senator Specter's role. Whoever is getting a raw deal now, or would get a better or worse deal under new legislation, the victims of asbestos are not now and never will be made whole.
However, there is a bit of data on asbestos, silica, claims and x-rays. Michigan has a “Silicosis and Dust Disease Fund,” paid out of a tiny surcharge on workers compensation premiums. Employers who recognize a worker’s claim for silicosis may apply to this fund for reimbursement. In addition, Michigan has an occupational disease reporting law. Together, these provide something of a convenience sample of disease victims.
Two papers provide insight into the relationship of silica exposure – in the foundry environment – and asbestosis.
Am J Ind Med. 1998 Aug;34(2):197-201.
Asbestos-related x-ray changes in foundry workers.
Rosenman KD, Reilly MJ.
Michigan State University, Department of Medicine, East Lansing 48824-1316, USA.
Michigan has a statewide mandatory occupational disease reporting system. As part of that system, reports are received from hospital, physicians, death certificates, the worker's compensation bureau, and company medical departments. Based on this reporting, the State of Michigan has a special emphasis program for the surveillance of silicosis, a known disease outcome among foundry workers. From 1985-1996, 115 cases reported to the State Surveillance System as silicosis, pneumoconiosis not specified, or pulmonary fibrosis were reclassified as having asbestos related x-ray changes after a B-reader interpretation of each case's chest x-ray. During this same period there were an additional 697 reports confirmed as silicosis and 6,724 cases reported to the surveillance system as asbestosis. Among the 115 reports reclassified as having asbestos-related x-ray changes without evidence of silicosis-related x-ray changes, 54 had worked in foundries. Only 7 (14.8%) of these individuals had their primary work in maintenance in the foundry; 40 (85.1%) had their primary foundry work in a production job; and for 10 individuals the occupation was not known. Asbestos has been used in foundries on pipe laggings, boiler coverings, as insulation in fan housings, in gloves, aprons and curtains, as insulation in cupolas, and in ladles and insulation in sand molds. Clinicians caring for foundry workers need to be aware that asbestos-related x-ray changes are not uncommon in this population and asbestos exposure should be considered as one of the carcinogens contributing to the known increased risk of lung cancer among foundry workers.>>>>>>>>>>>>>>>>>>>>>>>>>
Am J Epidemiol. 1996 Nov 1;144(9):890-900.
Silicosis among foundry workers. Implication for the need to revise the OSHA standard.
Rosenman KD, Reilly MJ, Rice C, Hertzberg V, Tseng CY, Anderson HA.
Department of Medicine, College of Human Medicine, Michigan State University, East Lansing, USA.
[Note that College of Human Medicine is there to distinguish the faculty from the College of Veterinary Medicine.]
To evaluate the risk of pneumoconiosis among workers in a Midwestern automotive foundry, medical records and silica sand exposure data were analyzed for 1,072 current and retired employees with at least 5 years of employment as of June 1991. Approximately half of these employees had worked at the foundry for 20 or more years. Sixty workers were found to have radiographic evidence of pneumoconiosis. Twenty-eight workers had radiographs consistent with silicosis, of which 25 were consistent with simple silicosis and three with progressive massive fibrosis. The prevalence of radiographic changes consistent with silicosis increased with: number of years worked at the foundry (6% for 20-29 years and 12% for 30 or more years); cigarette smoking (12.2% among smokers with high silica exposure vs. 4.4% among never smokers with high silica exposure); work area within the foundry (cleaning room, core room, mold area, core knockout); and quantitative silica exposure (0.3-2.7% of workers at the current Occupational Safety and Health Administration (OSHA) standard and 4.9-9.9% of workers above the OSHA standard). In addition, the odds of developing radiographic changes consistent with silicosis were increased for African Americans (odds ratio = 2.14, 95% confidence interval 0.85-5.60) in comparison with whites. (The risk was similar when silica exposure was equal, but African-American workers on average had greater exposure to silica, despite having a similar duration of work as white workers.) Another eight workers had radiographic evidence of asbestosis, and 24 had pleural plaques. These asbestos-related changes were not associated with increasing exposure to silica but rather were associated with being in the maintenance department and performing repair work. After controlling for cigarette smoking, race, and exposure to silica at another job besides the foundry, the authors found a 1.45 increased risk of developing a radiograph consistent with silicosis after 20 years of work at the current OSHA standard, and a 2.10 increased risk after 40 years of work at the current OSHA standard. On the basis of these findings, the authors recommend maintaining silica air levels no higher than the exposure level of 0.05 mg/m3 recommended by the National Institute for Occupational Safety and Health.
Specter Suggests Limiting State Silica Suits to Prevent Dual Filings
"Reacting to new testimony that asbestos- and silica-related disease are easy to distinguish, Senate Judiciary Committee Chairman Specter (R-Pa.) says lawmakers should now be able to draft language in a multibillion-dollar asbestos trust fund bill to prevent asbestos claimants from recasting their claims to refer to other harmful substances, such as silica. "There is no confusing asbestos and silica-related disease," Specter says after a hearing on the issue of "mixed dust" claims. "That should leave us a clear path to eliminate second claims" of asbestos claimants in court. "
>>>>>>>>>>>>>>>>>>>>>>>>>>>>
BrooklynDodger is not going to take a position here on asbestos compensation legislation or Senator Specter's role. Whoever is getting a raw deal now, or would get a better or worse deal under new legislation, the victims of asbestos are not now and never will be made whole.
However, there is a bit of data on asbestos, silica, claims and x-rays. Michigan has a “Silicosis and Dust Disease Fund,” paid out of a tiny surcharge on workers compensation premiums. Employers who recognize a worker’s claim for silicosis may apply to this fund for reimbursement. In addition, Michigan has an occupational disease reporting law. Together, these provide something of a convenience sample of disease victims.
Two papers provide insight into the relationship of silica exposure – in the foundry environment – and asbestosis.
Am J Ind Med. 1998 Aug;34(2):197-201.
Asbestos-related x-ray changes in foundry workers.
Rosenman KD, Reilly MJ.
Michigan State University, Department of Medicine, East Lansing 48824-1316, USA.
Michigan has a statewide mandatory occupational disease reporting system. As part of that system, reports are received from hospital, physicians, death certificates, the worker's compensation bureau, and company medical departments. Based on this reporting, the State of Michigan has a special emphasis program for the surveillance of silicosis, a known disease outcome among foundry workers. From 1985-1996, 115 cases reported to the State Surveillance System as silicosis, pneumoconiosis not specified, or pulmonary fibrosis were reclassified as having asbestos related x-ray changes after a B-reader interpretation of each case's chest x-ray. During this same period there were an additional 697 reports confirmed as silicosis and 6,724 cases reported to the surveillance system as asbestosis. Among the 115 reports reclassified as having asbestos-related x-ray changes without evidence of silicosis-related x-ray changes, 54 had worked in foundries. Only 7 (14.8%) of these individuals had their primary work in maintenance in the foundry; 40 (85.1%) had their primary foundry work in a production job; and for 10 individuals the occupation was not known. Asbestos has been used in foundries on pipe laggings, boiler coverings, as insulation in fan housings, in gloves, aprons and curtains, as insulation in cupolas, and in ladles and insulation in sand molds. Clinicians caring for foundry workers need to be aware that asbestos-related x-ray changes are not uncommon in this population and asbestos exposure should be considered as one of the carcinogens contributing to the known increased risk of lung cancer among foundry workers.>>>>>>>>>>>>>>>>>>>>>>>>>
Am J Epidemiol. 1996 Nov 1;144(9):890-900.
Silicosis among foundry workers. Implication for the need to revise the OSHA standard.
Rosenman KD, Reilly MJ, Rice C, Hertzberg V, Tseng CY, Anderson HA.
Department of Medicine, College of Human Medicine, Michigan State University, East Lansing, USA.
[Note that College of Human Medicine is there to distinguish the faculty from the College of Veterinary Medicine.]
To evaluate the risk of pneumoconiosis among workers in a Midwestern automotive foundry, medical records and silica sand exposure data were analyzed for 1,072 current and retired employees with at least 5 years of employment as of June 1991. Approximately half of these employees had worked at the foundry for 20 or more years. Sixty workers were found to have radiographic evidence of pneumoconiosis. Twenty-eight workers had radiographs consistent with silicosis, of which 25 were consistent with simple silicosis and three with progressive massive fibrosis. The prevalence of radiographic changes consistent with silicosis increased with: number of years worked at the foundry (6% for 20-29 years and 12% for 30 or more years); cigarette smoking (12.2% among smokers with high silica exposure vs. 4.4% among never smokers with high silica exposure); work area within the foundry (cleaning room, core room, mold area, core knockout); and quantitative silica exposure (0.3-2.7% of workers at the current Occupational Safety and Health Administration (OSHA) standard and 4.9-9.9% of workers above the OSHA standard). In addition, the odds of developing radiographic changes consistent with silicosis were increased for African Americans (odds ratio = 2.14, 95% confidence interval 0.85-5.60) in comparison with whites. (The risk was similar when silica exposure was equal, but African-American workers on average had greater exposure to silica, despite having a similar duration of work as white workers.) Another eight workers had radiographic evidence of asbestosis, and 24 had pleural plaques. These asbestos-related changes were not associated with increasing exposure to silica but rather were associated with being in the maintenance department and performing repair work. After controlling for cigarette smoking, race, and exposure to silica at another job besides the foundry, the authors found a 1.45 increased risk of developing a radiograph consistent with silicosis after 20 years of work at the current OSHA standard, and a 2.10 increased risk after 40 years of work at the current OSHA standard. On the basis of these findings, the authors recommend maintaining silica air levels no higher than the exposure level of 0.05 mg/m3 recommended by the National Institute for Occupational Safety and Health.
Tuesday, February 01, 2005
List of Cancer-Causing Agents Grows
The Department of Health and Human Services released its Eleventh Edition of the Report on Carcinogens on January 31, 2005, adding seventeen substances to the growing list of US recognized cancer-causing agents, bringing the total to 246.
"Among U.S. residents, 1 in 2 men and 1 in 3 women will develop cancer at some point in their lifetimes. Research shows that environmental factors trigger diseases like cancer" said Kenneth Olden, Ph.D., outgoing director of the National Institute of Environmental Health Sciences and the National Toxicology Program, which prepared the report for HHS.
The Report on Carcinogens, Eleventh Edition, referred to as the "RoC," lists cancer-causing agents in two categories -- "known to be human carcinogens" and "reasonably anticipated to be human carcinogens." The report now contains 58 "known" and 188 "reasonably anticipated" listings.
Six substances have been added to the "known" category. One newly added listing has occupational importance:
Hepatitis B virus (HBV) and hepatitis C virus (HCV) are viruses that cause acute or chronic liver disease. They are listed in the report as "known human carcinogens" because studies in people show that chronic hepatitis B and hepatitis C infections cause liver cancer. Infections can be prevented by reducing contact with contaminated fluids in health care settings and, for hepatitis B, by vaccination.
Already listed known human carcinogens of occupational significance include: Arsenic Compounds; Inorganic arsenic; Asbestos; Benzene; Beryllium and Beryllium Compounds; 1,3-Butadiene; Cadmium and Cadmium Compounds; Chromium Hexavalent Compounds; Coal Tar Pitches; Coal Tars; Coke Oven Emissions; Ethylene Oxide; Mineral Oils (Untreated and Mildly Treated); Nickel Compounds Silica, Crystalline (Respirable Size); Soots; Strong Inorganic Acid Mists Containing Sulfuric Acid; Vinyl Chloride; and Wood Dust.
Eleven substances have been added to the "reasonably anticipated" category. Those of occupational importance include:
Naphthalene which may be present in petroleum oils. Naphthalene is listed in the report as "reasonably anticipated to be a human carcinogen," based on inhalation studies in animals which showed it causes nasal tumors in rats and lung tumors in female mice.
Lead is used to make lead-acid storage batteries, lead compounds are used in paint, glass and ceramics, fuel additives. It is a widespread contaminant. The report lists lead and lead compounds as "reasonably anticipated to be human carcinogens" because exposure to lead or lead compounds is associated with an increased risk for lung or stomach cancer in humans, and cancer of the kidney, brain or lung in studies with laboratory animals.
Cobalt Sulfate is used in electroplating, as coloring agents for ceramics, and as drying agents in inks and paints. Cobalt sulfate is listed as "reasonably anticipated to be a human carcinogen" based on inhalation studies in laboratory animals that showed it causes adrenal gland and lung tumors.
Nitromethane is used in specialized fuels. It is listed as "reasonably anticipated to be a human carcinogen" based on evidence that it causes cancer in experimental animals.
The Report on Carcinogens, Eleventh Edition, is prepared by the National Toxicology Program, an interagency group coordinated by the U.S. Department of Health and Human Services. The full report is available at the NTP website http://ntp.niehs.nih.gov/.
>>>>>>>>>>>>>>>>>>>>>>>>>>
BrooklynDodger points out that there are two major competing carcinogen lists, the NTP list quoted here in press release, and the International Agency for Research Against Cancer (IARC) list. The number of agents depends on how you count classes of chemicals – “lead compounds” can be a lot of chemicals. The IARC list is more inclusive than the NTP list, because the criteria are different.
BrooklynDodger notes that among the “known” compounds above, OSHA standards taking carcinogenicity into account are lacking for beryllium, nickel, silica, sulfuric acid mist and wood dust, and now going into the hearing stage for chromates.
"Among U.S. residents, 1 in 2 men and 1 in 3 women will develop cancer at some point in their lifetimes. Research shows that environmental factors trigger diseases like cancer" said Kenneth Olden, Ph.D., outgoing director of the National Institute of Environmental Health Sciences and the National Toxicology Program, which prepared the report for HHS.
The Report on Carcinogens, Eleventh Edition, referred to as the "RoC," lists cancer-causing agents in two categories -- "known to be human carcinogens" and "reasonably anticipated to be human carcinogens." The report now contains 58 "known" and 188 "reasonably anticipated" listings.
Six substances have been added to the "known" category. One newly added listing has occupational importance:
Hepatitis B virus (HBV) and hepatitis C virus (HCV) are viruses that cause acute or chronic liver disease. They are listed in the report as "known human carcinogens" because studies in people show that chronic hepatitis B and hepatitis C infections cause liver cancer. Infections can be prevented by reducing contact with contaminated fluids in health care settings and, for hepatitis B, by vaccination.
Already listed known human carcinogens of occupational significance include: Arsenic Compounds; Inorganic arsenic; Asbestos; Benzene; Beryllium and Beryllium Compounds; 1,3-Butadiene; Cadmium and Cadmium Compounds; Chromium Hexavalent Compounds; Coal Tar Pitches; Coal Tars; Coke Oven Emissions; Ethylene Oxide; Mineral Oils (Untreated and Mildly Treated); Nickel Compounds Silica, Crystalline (Respirable Size); Soots; Strong Inorganic Acid Mists Containing Sulfuric Acid; Vinyl Chloride; and Wood Dust.
Eleven substances have been added to the "reasonably anticipated" category. Those of occupational importance include:
Naphthalene which may be present in petroleum oils. Naphthalene is listed in the report as "reasonably anticipated to be a human carcinogen," based on inhalation studies in animals which showed it causes nasal tumors in rats and lung tumors in female mice.
Lead is used to make lead-acid storage batteries, lead compounds are used in paint, glass and ceramics, fuel additives. It is a widespread contaminant. The report lists lead and lead compounds as "reasonably anticipated to be human carcinogens" because exposure to lead or lead compounds is associated with an increased risk for lung or stomach cancer in humans, and cancer of the kidney, brain or lung in studies with laboratory animals.
Cobalt Sulfate is used in electroplating, as coloring agents for ceramics, and as drying agents in inks and paints. Cobalt sulfate is listed as "reasonably anticipated to be a human carcinogen" based on inhalation studies in laboratory animals that showed it causes adrenal gland and lung tumors.
Nitromethane is used in specialized fuels. It is listed as "reasonably anticipated to be a human carcinogen" based on evidence that it causes cancer in experimental animals.
The Report on Carcinogens, Eleventh Edition, is prepared by the National Toxicology Program, an interagency group coordinated by the U.S. Department of Health and Human Services. The full report is available at the NTP website http://ntp.niehs.nih.gov/.
>>>>>>>>>>>>>>>>>>>>>>>>>>
BrooklynDodger points out that there are two major competing carcinogen lists, the NTP list quoted here in press release, and the International Agency for Research Against Cancer (IARC) list. The number of agents depends on how you count classes of chemicals – “lead compounds” can be a lot of chemicals. The IARC list is more inclusive than the NTP list, because the criteria are different.
BrooklynDodger notes that among the “known” compounds above, OSHA standards taking carcinogenicity into account are lacking for beryllium, nickel, silica, sulfuric acid mist and wood dust, and now going into the hearing stage for chromates.
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