A sub-acute inhalation study of effects of MWF in the laboratory was published by colleagues in Korea. BrooklynDodger takes the challenge of extrapolating risk from brief exposures to small numbers of rats to that for thousands of people exposed for years. According to the investigators:
Rats were exposed a 10 mg/m(3) concentration of metalworking fluid (MWF) [without added endotoxin] and contaminated with endotoxin at concentrations of 1813 (low dose) and 20,250 eu/m(3) (high dose) 6 hr per day for 8 weeks [not clear how many rats per group; this effects statistical significance, imporant for the control group]. ...Lung weight increased significantly in the rats exposed to the MWF both with and without endotoxins. ... The NOx production activity of the BAL cells increased significantly in the rats exposed to the MWF with and without endotoxins. Increases in lung weight, number of PMN cells, and levels of extracellular cytokines and NOx were all more significant in the rats exposed to the MWF with endotoxins rather than in those exposed to MWF without endotoxins. [but still increased in the MWF only exposed rats.] In spleen cell cultures, T-cell proliferation activity was decreased... after repeated exposure to MWF with and without endotoxins....
The investigators described the fluid as: Loca emulsion oil (Shell, Korea) was selected as the watersolubleMWF because it includes few additives and is popularly used in Korea. Mineral oil constituted 80.0%–90.0% ofthe MWF (Cas. No. 64742-55-8) and 2-octyl-3-isothiazolone was less than 1% (Cas. No. 26530-20-1). No nitrosamines, formaldehyde, or ethanolamines [were detected.]
Debates about MWF health effects include the role of microbial products in respiratory effects. Endotoxin, derived from the corpses of gram negative bacteria which routinely grow in MWF, clearly contributes to effects seen in laboratory studies; it's not surprising that endotoxin by itself damages lungs. This study demonstrates that fluid without added endotoxin, apparently made up directly from concentrate, also damages lungs under these exposure circumstances. The investigators neglected to identify the emulsifier [likely a petroleum sulfonate] surely present in the formulation, and any non-ionic surfactant which might have been included. The aerosol was apparently a 5% dilution of concentrate; for mass measurements, the water part of the aerosol goes away, but the animal's respiratory systems saw droplets with typical workplace concentrations.
BrooklynDodger concludes that 10 mg/M3 is a sub-chronic effect level for a bland soluble oil uncontaminated with endotoxin, causing increased lung weight and a variety of indicators of inflammation. BrooklynDodger would appy extrapolation factors for AEL to NOAEL, for NOAEL [10% effect] to an acceptable risk rate, and for sub-chronic to chronic to identify a reference dose. For IRIS purposes, EPA's default would be 10 fold for each. Using a much less risk adverse factor of 5 for each, BrooklynDodger derives a reference dose of 0.1 mg/M3 for mild soluble oil uncontaminated with endotoxin.
>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
Environ Toxicol. 2005 Apr;20(2):212-8.
Inflammatory and immunological responses to subchronic exposure to endotoxin-contaminated metalworking fluid aerosols in F344 rats.
Lim CH, Yu IJ, Kim HY, Lee SB, Kang MG, Marshak DR, Moon CK.Center for Occupational Toxicology, Occupational Safety and Health Research Institute, Korea Occupational Safety and Health Agency, Daejeon, South Korea.
Sunday, May 29, 2005
Saturday, May 28, 2005
Ergonomics - Who's the Expert? Ask the person doing the job.
The current problem in ergonomics for manufacturing jobs is that most jobs are rated "moderate" by risk assessment methods. Most MSD injuries come from these moderate jobs, and appear randomly across this stratum. Is this because the risk assessment tools are not distinguishing risk? Or, do all the jobs have to be abated in no particular order. This U of M Center for Ergonomics may shed some light.
Eight analysts observed 32 subjects and estimated force as a percent of subjects' maximum voluntary contraction (% MVC). High force exertions (> 67% MVC) were underestimated and low force exertions (<34%> were overestimated. Because forceful exertions often lack conspicuous, visual cues that indicate the magnitude of the exertion, it is recommended that the individuals who actually perform the activity provide feedback when evaluating force."
BrooklynDodger thinks the problem is observing hand and wrist posture. Ergonomic risk is understood by the force, frequency, posture, duration paradigm. In this listing "force" is external force applied on objects by the worker. But the damage is done by the internal force applied by the muscle to some body structure. The force the muscle must apply internally is a function of the external force and the joint posture. Posture of the back and the shoulder are relatively easy to observe: these body parts are large and don't move that fast. Not so the hand and wrist.
The Dodger expects these observers were not biased by management wanting the jobs to pass the analysis. They weren't consultants fearing loss of the contract if they flunk too many jobs, or flunk jobs where the workers aren't complaining. They weren't biased by knowing there had been an injury and wanting to flunk the job. They likely were biased by not wanting to be too far off the evaluations by their peers. Which means rating the job really bad when most observers rated it really good, or the opposite. This would have biased observations to the mean, as observed.
Now that science - at least one study which should be replicated - suggests that the worker doing the job knows best, how to implement?
J Occup Rehabil. 2004 Dec;14(4):281-94.
Observational assessment of forceful exertion and the perceived force demands of daily activities.
Marshall MM, Armstrong TJ.
Department of Industrial and Systems Engineering, Rochester Institute of Technology, Rochester, New York 14623, USA. mmmeie@rit.edu
Eight analysts observed 32 subjects and estimated force as a percent of subjects' maximum voluntary contraction (% MVC). High force exertions (> 67% MVC) were underestimated and low force exertions (<34%> were overestimated. Because forceful exertions often lack conspicuous, visual cues that indicate the magnitude of the exertion, it is recommended that the individuals who actually perform the activity provide feedback when evaluating force."
BrooklynDodger thinks the problem is observing hand and wrist posture. Ergonomic risk is understood by the force, frequency, posture, duration paradigm. In this listing "force" is external force applied on objects by the worker. But the damage is done by the internal force applied by the muscle to some body structure. The force the muscle must apply internally is a function of the external force and the joint posture. Posture of the back and the shoulder are relatively easy to observe: these body parts are large and don't move that fast. Not so the hand and wrist.
The Dodger expects these observers were not biased by management wanting the jobs to pass the analysis. They weren't consultants fearing loss of the contract if they flunk too many jobs, or flunk jobs where the workers aren't complaining. They weren't biased by knowing there had been an injury and wanting to flunk the job. They likely were biased by not wanting to be too far off the evaluations by their peers. Which means rating the job really bad when most observers rated it really good, or the opposite. This would have biased observations to the mean, as observed.
Now that science - at least one study which should be replicated - suggests that the worker doing the job knows best, how to implement?
J Occup Rehabil. 2004 Dec;14(4):281-94.
Observational assessment of forceful exertion and the perceived force demands of daily activities.
Marshall MM, Armstrong TJ.
Department of Industrial and Systems Engineering, Rochester Institute of Technology, Rochester, New York 14623, USA. mmmeie@rit.edu
Friday, May 27, 2005
Does exercise increase the risk of knee OA
Since CDC wants us to exercise, it's worth thinking about other risks. This paper is a random survey of England. Extracted conclusions were
From 4316 people originally interviewed, 216 eligible cases (66 men, 150 women) were identified (mean age 57.1). [about 5% of this random sample of England.] Each case was matched to four controls. When habitual sport/exercise participation were examined during a subject's life, only exposure to regular long walks and being physically active between the ages of 20 and 24 suggested any association with developing knee OA later in life. The only strong association found was a greatly increased risk of knee OA having previously sustained a knee injury (odds ratio 8.0)
The Dodger actually didn't read the full text with great enthusiasm. This was retrospective assessment, so the rate of OA is prevalence and not stratified by age. The Dodger remembers they collected BMI information, so they must have asked about smoking too, but reported no association with OA. There appeared to be no consideration of occupational activity, only physical fitness stuff. There's no data about activity during 40% of waking hours. Plus, the Dodger imagines that persons with physically demanding jobs may be less likely to play squash on their off hours, which would introduce negative confounding with risks of exercise.
Ann Rheum Dis. 2001 Aug;60(8):756-64.
A case-control study to investigate the relation between low and moderate levels of physical activity and osteoarthritis of the knee using data collected as part of the Allied Dunbar National Fitness Survey.
Sutton AJ, Muir KR, Mockett S, Fentem P.Department of Epidemiology and Public Health, University of Leicester, 22-28 Princess Road West, Leicester LE1 6TP, UK. ajs22@le.ac.uk
From 4316 people originally interviewed, 216 eligible cases (66 men, 150 women) were identified (mean age 57.1). [about 5% of this random sample of England.] Each case was matched to four controls. When habitual sport/exercise participation were examined during a subject's life, only exposure to regular long walks and being physically active between the ages of 20 and 24 suggested any association with developing knee OA later in life. The only strong association found was a greatly increased risk of knee OA having previously sustained a knee injury (odds ratio 8.0)
The Dodger actually didn't read the full text with great enthusiasm. This was retrospective assessment, so the rate of OA is prevalence and not stratified by age. The Dodger remembers they collected BMI information, so they must have asked about smoking too, but reported no association with OA. There appeared to be no consideration of occupational activity, only physical fitness stuff. There's no data about activity during 40% of waking hours. Plus, the Dodger imagines that persons with physically demanding jobs may be less likely to play squash on their off hours, which would introduce negative confounding with risks of exercise.
Ann Rheum Dis. 2001 Aug;60(8):756-64.
A case-control study to investigate the relation between low and moderate levels of physical activity and osteoarthritis of the knee using data collected as part of the Allied Dunbar National Fitness Survey.
Sutton AJ, Muir KR, Mockett S, Fentem P.Department of Epidemiology and Public Health, University of Leicester, 22-28 Princess Road West, Leicester LE1 6TP, UK. ajs22@le.ac.uk
Human Variability - increased low dose risk
A shallow slope of the exposure response relationship in the observable range in a laboratory bioassay predicts a higher low dose risk; a steep slope a lower low dose risk and thus allows a higher and less protective exposure limit. Increased variability in biological response of the host predicts a shallower exposure response relationship. BrooklynDodger hypothesizes that genetically diverse free living humans show greater variability than genetically homogeneous inbred laboratory housed animals. Therefore, a reference dose established with a dose response relationship in a laboratory study will be underestimate risk in people.
Studies identifying human variability in biological response are important to compare to similar variability in laboratory animals.
Which brings the Dodger to a study of an old favorite chemical, parathion, an organophosphate pesticide. Parathion [ethyl parathion] and methyl parathion, its less toxic to mammals cousin, interest because of competing intoxication and detoxification pathways. For each, the parent compound is oxidized to the corresponding paraoxon, the cholinesterase inhibitor. Parent compound and oxon may be dealkylated. Paraoxonase hydrolyzes and detoxifies the oxon. Concentration of oxon is determined by equilibrium of intoxication and detoxification; biological effect is fraction of cholinesterase inhibition.
Anyway, that brings us to paraoxonase variability. Apparently fancy new techniques have identified 4 forms of paraoxonase, which has biological activity beyond OP detoxification [take that intelligent design advocates]. This study found 5-fold variation of activity toward one substrate, and 20-fold variation toward paraoxon.
Human paraoxonase (PON1) plays a role in detoxification of organophosphorus (OP) compounds by hydrolyzing the bioactive oxons... Some PON1 polymorphisms have been found to be responsible for variations in catalytic activity and expression and have been associated with susceptibility to OP poisoning and vascular diseases. ... The studied population consisted of unrelated individuals (n = 214)... We found a wide interindividual variability of PON1 activity with a unimodal distribution; the range of enzymatic activity toward phenylacetate was 84.72 to 422.0 U/mL, and 88.37 to 1645.6 U/L toward paraoxon.
Toxicology and Applied Pharmacology Volume 205, Issue 3 , 15 June 2005, Pages 282-289
Genetic polymorphisms and activity of PON1 in a Mexican population
A.E. Rojas-Garcíaa, M.J. Solís-Herediaa, B. Piña-Guzmána, L. Vegaa, L. López-Carrillob and B. Quintanilla-Vegaa, ,
aSección Externa de Toxicología, CINVESTAV-IPN, PO Box 14-740, Mexico City, 07300, MexicobInstituto Nacional de Salud Pública, Ave. Universidad No. 655, Col. Santa Ma. Ahuacatitlán, Cuernavaca, Mor., 62508, Mexico Received 18 August 2004; accepted 22 October 2004. Available online 8 December 2004.
Studies identifying human variability in biological response are important to compare to similar variability in laboratory animals.
Which brings the Dodger to a study of an old favorite chemical, parathion, an organophosphate pesticide. Parathion [ethyl parathion] and methyl parathion, its less toxic to mammals cousin, interest because of competing intoxication and detoxification pathways. For each, the parent compound is oxidized to the corresponding paraoxon, the cholinesterase inhibitor. Parent compound and oxon may be dealkylated. Paraoxonase hydrolyzes and detoxifies the oxon. Concentration of oxon is determined by equilibrium of intoxication and detoxification; biological effect is fraction of cholinesterase inhibition.
Anyway, that brings us to paraoxonase variability. Apparently fancy new techniques have identified 4 forms of paraoxonase, which has biological activity beyond OP detoxification [take that intelligent design advocates]. This study found 5-fold variation of activity toward one substrate, and 20-fold variation toward paraoxon.
Human paraoxonase (PON1) plays a role in detoxification of organophosphorus (OP) compounds by hydrolyzing the bioactive oxons... Some PON1 polymorphisms have been found to be responsible for variations in catalytic activity and expression and have been associated with susceptibility to OP poisoning and vascular diseases. ... The studied population consisted of unrelated individuals (n = 214)... We found a wide interindividual variability of PON1 activity with a unimodal distribution; the range of enzymatic activity toward phenylacetate was 84.72 to 422.0 U/mL, and 88.37 to 1645.6 U/L toward paraoxon.
Toxicology and Applied Pharmacology Volume 205, Issue 3 , 15 June 2005, Pages 282-289
Genetic polymorphisms and activity of PON1 in a Mexican population
A.E. Rojas-Garcíaa, M.J. Solís-Herediaa, B. Piña-Guzmána, L. Vegaa, L. López-Carrillob and B. Quintanilla-Vegaa, ,
aSección Externa de Toxicología, CINVESTAV-IPN, PO Box 14-740, Mexico City, 07300, MexicobInstituto Nacional de Salud Pública, Ave. Universidad No. 655, Col. Santa Ma. Ahuacatitlán, Cuernavaca, Mor., 62508, Mexico Received 18 August 2004; accepted 22 October 2004. Available online 8 December 2004.
Thursday, May 26, 2005
Money Tox - Pharma Walks
BrooklynDodger fumes at this inadequate study cluttering the abstractosphere [medline] with an uniformative null finding aimed at reducing concern for occupational exposures in the pharma industry. The Dodger hopes reviewers and editors will step up to responsibility in this matter, because careers are built on paper counts, not necesarily paper content.
The Dodger has posted the abstract in full below, so as to allow the gentle reader to note what was put in the full text but left out here.
Other than drawing null conclusions from an inadequate study, the investigators display a new trick to enhance and then ignore the healthy worker effect. By mixing salaried with hourly workers [or, professional, executive, administrative and clerical with operatives and service personnel] for cohort analyses, and then ignoring them for exposure response analyses, the investigators are able to sweep any possible work related associations under the rug.
The paper is published with no attribution of funding or statement on conflict in the end matter. The text notes "In 1995, the company commissioned us to design and conduct the study." Obviously there's a conflict which should be disclosed in the end matter: the degree of conflict would be reduced were the investigators selected by competitive application and independent peer review.
The Dodger notes that the same PI has published on a cohort from Merck, and wonders if the paper here is an offshoot of the larger other study. The Dodger can't resist noting the proud history of disclosing health issues in Merck's core business: Merck's Vioxx Liability Could Reach $38 Billion - Forbes.com... a result of taking Vioxx were to receive an average-sized legal settlement,Evans wrote in a research report, Merck's liability could reach $38 billion. ...www.forbes.com/markets/bonds/ 2004/12/03/1203automarketscan13.html The Dodger will revisit the 50 year study in a later post.
J Occup Environ Med. 2004 Feb;46(2):161-6.
A 50-year historical cohort mortality study of workers in a pharmaceutical plant.
Dolan DG, Youk AO, Marsh GM, Buchanich JM.Merck & Company, Inc, Whitehouse Station, NJ 08889-0200, USA. david_dolan@merck.com
Having digressed, the Dodger returns to the study at hand.
The fatal flaw of this investigation was that only 112 or 5.6% of the total cohort was identified as deceased. They disclose and all cause SMR of 64 for the whole cohort, which approaches the world record low SMR. The SMR is a product of short observation, any employment related effect would have to come from comparing groups within the cohort, and with 112 cases total there's little change to do exposure response. However, comparing the part of the cohort who worked in production areas to those who didn't, the all-cause SMRs are 46 vs. 71 for production areas [which, the Dodger suspects, includes engineers and supervisors]. The Dodger would bet 50 cents that the increased mortality suffered by compared to salaried in this cohort achieved statistical significance.
The main finding in this study designed not to find anything, is 4 cases of non-Hodgkins Lymphoma, SMR = 307, marginally significant in the production cohort. This is compared to no cases of this disease in the office cohort. For exposure response analyses, the office cohort was excluded from the zero exposure group, attenuating measures of association. All these victims cam from among workers with at least 10 years of employment, and the SMR = 584 among those with 20 years since hire [a surrogate for latency from first exposure] was statistically significant.
The investigators say "we developed individual worker-level, multi-exposure profiles for all plant exposure agents with available air monitoring data (acetone, aceto-nitrile, di-methyl formamide, ethyl acetate, ethylene di-chloride, isopropyl alcohol, methlyene chloride, tri-chloroethane, and toluene)." Sounds like cranking the cash register on a grab bag of solvents, average exposure under 10 ppm, median exposures zero for several. MC, EDC and DMF are of some interest but not at these levels. The only shred of scientific merit in this effort would be effects of the product, but the product or class of product is not disclosed. Are they making birth control pills, viagra, anti-neoplastic agents, or are they packaging Tums?
Bottom line and new rules.
1. Abstracts should state whether study was adequate to address the goal of the study. In this case, the study was inadequate to support a null hypothesis that chemical exposures in the facility were not causing increase mortality.
2. Null results from inadequate studies should have no weight in risk assessment.
3. Associations revealed by inadequate studies should have some weight in risk assessment; these associations should not be discounted by failure to observe an exposure response relationship.
4. Publishing an SMR of salaried and hourly employees combined misleads the literature.
>>>>>>>>>>>>>>>>>>>>>>>>
Ann Epidemiol. 2005 Feb;15(2):112-22.
Mortality patterns among workers in a US pharmaceutical production plant.
Marsh GM, Youk AO, Esmen NA, Buchanich JM.Department of Biostatistics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA 15261, USA. gmarsh@pitt.edu
PURPOSE: To examine mortality among workers in a pharmaceutical production plant and to address community concerns about 1980 to 1990 increases in local county cancer mortality rates. METHODS: Subjects were 1999 workers with some full-time employment during the period between 1970 and 1996. We identified deaths through the year 2000 and reconstructed exposures to nine chemical agents with available exposure measurements. Data analyses included standardized mortality ratios (SMRs) and time trends in local cancer mortality rates. RESULTS: We observed deficits in deaths from all causes combined, all cancers combined, and most cause of death categories examined. Male workers with potential plant exposure had excesses in deaths from all lymphatic-hematopoietic tissue cancers (LHTC), in particular non-Hodgkin's lymphoma (NHL), and respiratory system cancers (RSC) that were larger among long-term workers, but the pattern of findings suggested the excesses were probably not related to occupational factors at the plant. The increase in local county cancer mortality rates was simply the upward cycle of a periodic trend that peaked in 1990 and returned to 1980 levels in 2000. CONCLUSIONS: With the possible exceptions of LHTC, in particular NHL, and RSC, this study provided no evidence of elevated total or cause-specific cohort mortality risks. It does not appear that plant factors played a role in the 1980 to 1990 increases in local county cancer mortality rates.
The Dodger has posted the abstract in full below, so as to allow the gentle reader to note what was put in the full text but left out here.
Other than drawing null conclusions from an inadequate study, the investigators display a new trick to enhance and then ignore the healthy worker effect. By mixing salaried with hourly workers [or, professional, executive, administrative and clerical with operatives and service personnel] for cohort analyses, and then ignoring them for exposure response analyses, the investigators are able to sweep any possible work related associations under the rug.
The paper is published with no attribution of funding or statement on conflict in the end matter. The text notes "In 1995, the company commissioned us to design and conduct the study." Obviously there's a conflict which should be disclosed in the end matter: the degree of conflict would be reduced were the investigators selected by competitive application and independent peer review.
The Dodger notes that the same PI has published on a cohort from Merck, and wonders if the paper here is an offshoot of the larger other study. The Dodger can't resist noting the proud history of disclosing health issues in Merck's core business: Merck's Vioxx Liability Could Reach $38 Billion - Forbes.com... a result of taking Vioxx were to receive an average-sized legal settlement,Evans wrote in a research report, Merck's liability could reach $38 billion. ...www.forbes.com/markets/bonds/ 2004/12/03/1203automarketscan13.html The Dodger will revisit the 50 year study in a later post.
J Occup Environ Med. 2004 Feb;46(2):161-6.
A 50-year historical cohort mortality study of workers in a pharmaceutical plant.
Dolan DG, Youk AO, Marsh GM, Buchanich JM.Merck & Company, Inc, Whitehouse Station, NJ 08889-0200, USA. david_dolan@merck.com
Having digressed, the Dodger returns to the study at hand.
The fatal flaw of this investigation was that only 112 or 5.6% of the total cohort was identified as deceased. They disclose and all cause SMR of 64 for the whole cohort, which approaches the world record low SMR. The SMR is a product of short observation, any employment related effect would have to come from comparing groups within the cohort, and with 112 cases total there's little change to do exposure response. However, comparing the part of the cohort who worked in production areas to those who didn't, the all-cause SMRs are 46 vs. 71 for production areas [which, the Dodger suspects, includes engineers and supervisors]. The Dodger would bet 50 cents that the increased mortality suffered by compared to salaried in this cohort achieved statistical significance.
The main finding in this study designed not to find anything, is 4 cases of non-Hodgkins Lymphoma, SMR = 307, marginally significant in the production cohort. This is compared to no cases of this disease in the office cohort. For exposure response analyses, the office cohort was excluded from the zero exposure group, attenuating measures of association. All these victims cam from among workers with at least 10 years of employment, and the SMR = 584 among those with 20 years since hire [a surrogate for latency from first exposure] was statistically significant.
The investigators say "we developed individual worker-level, multi-exposure profiles for all plant exposure agents with available air monitoring data (acetone, aceto-nitrile, di-methyl formamide, ethyl acetate, ethylene di-chloride, isopropyl alcohol, methlyene chloride, tri-chloroethane, and toluene)." Sounds like cranking the cash register on a grab bag of solvents, average exposure under 10 ppm, median exposures zero for several. MC, EDC and DMF are of some interest but not at these levels. The only shred of scientific merit in this effort would be effects of the product, but the product or class of product is not disclosed. Are they making birth control pills, viagra, anti-neoplastic agents, or are they packaging Tums?
Bottom line and new rules.
1. Abstracts should state whether study was adequate to address the goal of the study. In this case, the study was inadequate to support a null hypothesis that chemical exposures in the facility were not causing increase mortality.
2. Null results from inadequate studies should have no weight in risk assessment.
3. Associations revealed by inadequate studies should have some weight in risk assessment; these associations should not be discounted by failure to observe an exposure response relationship.
4. Publishing an SMR of salaried and hourly employees combined misleads the literature.
>>>>>>>>>>>>>>>>>>>>>>>>
Ann Epidemiol. 2005 Feb;15(2):112-22.
Mortality patterns among workers in a US pharmaceutical production plant.
Marsh GM, Youk AO, Esmen NA, Buchanich JM.Department of Biostatistics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA 15261, USA. gmarsh@pitt.edu
PURPOSE: To examine mortality among workers in a pharmaceutical production plant and to address community concerns about 1980 to 1990 increases in local county cancer mortality rates. METHODS: Subjects were 1999 workers with some full-time employment during the period between 1970 and 1996. We identified deaths through the year 2000 and reconstructed exposures to nine chemical agents with available exposure measurements. Data analyses included standardized mortality ratios (SMRs) and time trends in local cancer mortality rates. RESULTS: We observed deficits in deaths from all causes combined, all cancers combined, and most cause of death categories examined. Male workers with potential plant exposure had excesses in deaths from all lymphatic-hematopoietic tissue cancers (LHTC), in particular non-Hodgkin's lymphoma (NHL), and respiratory system cancers (RSC) that were larger among long-term workers, but the pattern of findings suggested the excesses were probably not related to occupational factors at the plant. The increase in local county cancer mortality rates was simply the upward cycle of a periodic trend that peaked in 1990 and returned to 1980 levels in 2000. CONCLUSIONS: With the possible exceptions of LHTC, in particular NHL, and RSC, this study provided no evidence of elevated total or cause-specific cohort mortality risks. It does not appear that plant factors played a role in the 1980 to 1990 increases in local county cancer mortality rates.
Wednesday, May 25, 2005
Arthritis Month - Ignoring Root Causes (I)
BrooklynDodger found an interesting post relevent to ergonomics on the Occupational Medicine listserve:
Original post [summary];
Notice to Readers: National Arthritis Month --- May 2005
May is National Arthritis Month. This year, the Arthritis Foundation is urging persons with arthritis to get active for better health. [actually, recommendations look to be for preventing arthritis] Regular moderate physical activity improves the health and function of joints and reduces the risk for other chronic conditions. Physical activity helps protect joints by strengthening muscles and improving balance and joint nutrition, which leads to better flexibility, joint motion, and physical function. Long-term benefits include reduced pain, improvedmental health, and delayed disability (1). Walking is an ideal activity for most persons with arthritis because itis low impact, can be incorporated into usual daily activities, and does not require special equipment or facilities. A free copy of the Arthritis Today Walking Guide is available at http://www.arthritis.org. CDC, along with 36 state arthritisprograms, the Arthritis Foundation, and other organizations, continue toimplement the National Arthritis Action Plan.
National arthritis action plan: a public healthstrategy. Atlanta, GA: Arthritis Foundation; 1999. Available athttp://www.cdc.gov/nccdphp/pdf/naap.pdf.
What was missing was ergonomics and occupational exposure. The reply to the list serve noted
"I was irritated enough to download the Arthritis Foundation action plan and
skim it. The plan does mention occupational injury in the middle of the
pack for causes of arthritis, maybe as much as half a page in a 64 page
document, with no action items related.
"This is the same old same old blame the victim, exhortation approach to
public health which dominates all CDC health communications. Although
the action plan mentions "primary prevention," it's mostly obesity and
exercise. Scientifically, it would be nice if CDC would calculate
whether routine factory and construction work, for example, meet their
guidelines for exercise. Before they dog people who are pounding steel
10 hours on the assembly line for not training for marathons afterwards,
figure out how many METS are expended and whether they are meeting the
walking quota quoted below."
BrooklynDodger had recently posted a commentary showing that jobs with knee bending were associated with increased knee osteoarthritis. An acquaintance with bad knees told the Dodger that medical advice was that causes were hereditary, with no mention of occupation.
Maybe the Dodger's frustration with CDC and the Arthritis Foundation is misplaced. About 60% of the workforce is in executive, professional, administrative and technical jobs, mostly jobs with no special physical demands [other than prolonged static posture of the upper body.] About 18% of people are in operator and assembler jobs, and some of them are not specially stressful. So maybe occupational ergonomics is just left out because it's a minority's problem, and a less than elite minority as well.
Original post [summary];
Notice to Readers: National Arthritis Month --- May 2005
May is National Arthritis Month. This year, the Arthritis Foundation is urging persons with arthritis to get active for better health. [actually, recommendations look to be for preventing arthritis] Regular moderate physical activity improves the health and function of joints and reduces the risk for other chronic conditions. Physical activity helps protect joints by strengthening muscles and improving balance and joint nutrition, which leads to better flexibility, joint motion, and physical function. Long-term benefits include reduced pain, improvedmental health, and delayed disability (1). Walking is an ideal activity for most persons with arthritis because itis low impact, can be incorporated into usual daily activities, and does not require special equipment or facilities. A free copy of the Arthritis Today Walking Guide is available at http://www.arthritis.org. CDC, along with 36 state arthritisprograms, the Arthritis Foundation, and other organizations, continue toimplement the National Arthritis Action Plan.
National arthritis action plan: a public healthstrategy. Atlanta, GA: Arthritis Foundation; 1999. Available athttp://www.cdc.gov/nccdphp/pdf/naap.pdf.
What was missing was ergonomics and occupational exposure. The reply to the list serve noted
"I was irritated enough to download the Arthritis Foundation action plan and
skim it. The plan does mention occupational injury in the middle of the
pack for causes of arthritis, maybe as much as half a page in a 64 page
document, with no action items related.
"This is the same old same old blame the victim, exhortation approach to
public health which dominates all CDC health communications. Although
the action plan mentions "primary prevention," it's mostly obesity and
exercise. Scientifically, it would be nice if CDC would calculate
whether routine factory and construction work, for example, meet their
guidelines for exercise. Before they dog people who are pounding steel
10 hours on the assembly line for not training for marathons afterwards,
figure out how many METS are expended and whether they are meeting the
walking quota quoted below."
BrooklynDodger had recently posted a commentary showing that jobs with knee bending were associated with increased knee osteoarthritis. An acquaintance with bad knees told the Dodger that medical advice was that causes were hereditary, with no mention of occupation.
Maybe the Dodger's frustration with CDC and the Arthritis Foundation is misplaced. About 60% of the workforce is in executive, professional, administrative and technical jobs, mostly jobs with no special physical demands [other than prolonged static posture of the upper body.] About 18% of people are in operator and assembler jobs, and some of them are not specially stressful. So maybe occupational ergonomics is just left out because it's a minority's problem, and a less than elite minority as well.
Tuesday, May 24, 2005
More on bended knees, and shoe fetishes - reviewers and editors asleep at the switch
BrooklynDodger has been thinking about lower extremity disorders related to occupation. The Dodger found an adulterated [was going to say toxic] abstract of a paper with some interesting data.
Interviews in participants' homes of 29 cases identified from orthopaedic hospital surgical waiting list, and 83 controls identified by general practitioners were conducted. Women aged 50 to 70 years. Univariate analyses identified several significant associations with OAK including past knee injury, arthritis of the feet, heavy smoking, being overweight (BMI 25 or above) and various occupational activities. Virtually all measures of high heeled shoes use were associated with reduced risk of OAK, although none of these findings were statistically significant. In multivariate analysis only BMI 25 or above at age 36-40 remained significantly associated with OAK (OR 36.4, 95% CI 3.07 to 432), although weak evidence suggested certain occupational activities might increase risk. Being overweight before the age of 40 considerably increased the risk of subsequent symptomatic OAK in women. Wearing high heeled shoes did not.
Obviously, the Dodger is frosted about the "weak evidence" part. The authors also give us two more weasel works, "suggested" and "might" for what is really pretty good data given the limits of the study. First, this is a seriously underpowered study. Underpowered studies are usually condemned to uncertain results, but not necessarily "weak" results.
Second, the "weak" applies to the p value [as discussed below], not the risk ratio. The Dodger hates the term weak, but it conventionally applies to the risk ratio alone, with statistical uncertainty addressed with some other adjective.
The occupational activities were lifting, where a reported 24 to 33 years gave a significant risk ratio of 7.31; bending, where 21-33 years gave a signficant risk ratio of 12.36, and kneeling where 33 years plus gave a risk ratio of 4.18, cleaning floors on knees gave a risk ratio of 5.28. In each category the controls had substantially higher proportions in the lowest tertile than victims. There was falloff in risk ratio in the highest tertile of victims, plausibly explainable by disability related termination of exposure. None of these are "weak" associations.
Multivariate analysis gave a risk ratio for 21–34 years of bending of 12.91, with a upper limit of 167 (!!!), marginally significant. For 34 years, the risk ratio of 9.81 was not signficant, but upper limit was 125.
Lacking a plausible mechanism for smoking increasing OA, it is plausible that the increase of smoking among controls is caused by pain. The association of BMI with increased OA is mechanistically plausible, but increased BMI caused by pain may account for some of the association. Persons in industrial jobs are frequently selected for being big at the start, another source of uncontrolled confounding with a bias to the null. The cut point of BMI = 25 is equivalent to 155 pounds of weight for a 5'6" tall person, which is not exactly tubby.
Although Manolo Blahnik and shoe fetishists can take some comfort in these data, the Dodger would like to see the cross tabs for BMI and high heeled shoes, and occupational risk factors and high heeled shoes, to rule out confounding.
J Epidemiol Community Health. 2003 Oct;57(10):823-30.
An investigation of risk factors for symptomatic osteoarthritis of the knee in women using a life course approach.
Dawson J, Juszczak E, Thorogood M, Marks SA, Dodd C, Fitzpatrick R.Oxford Centre for Health Care Research and Development (OCHRAD) School of Health and Social Care, Oxford Brookes University, 44 London Road, Oxford OX3 7PD, UK. jdawson@brookes.ac.ukSTUDY
Interviews in participants' homes of 29 cases identified from orthopaedic hospital surgical waiting list, and 83 controls identified by general practitioners were conducted. Women aged 50 to 70 years. Univariate analyses identified several significant associations with OAK including past knee injury, arthritis of the feet, heavy smoking, being overweight (BMI 25 or above) and various occupational activities. Virtually all measures of high heeled shoes use were associated with reduced risk of OAK, although none of these findings were statistically significant. In multivariate analysis only BMI 25 or above at age 36-40 remained significantly associated with OAK (OR 36.4, 95% CI 3.07 to 432), although weak evidence suggested certain occupational activities might increase risk. Being overweight before the age of 40 considerably increased the risk of subsequent symptomatic OAK in women. Wearing high heeled shoes did not.
Obviously, the Dodger is frosted about the "weak evidence" part. The authors also give us two more weasel works, "suggested" and "might" for what is really pretty good data given the limits of the study. First, this is a seriously underpowered study. Underpowered studies are usually condemned to uncertain results, but not necessarily "weak" results.
Second, the "weak" applies to the p value [as discussed below], not the risk ratio. The Dodger hates the term weak, but it conventionally applies to the risk ratio alone, with statistical uncertainty addressed with some other adjective.
The occupational activities were lifting, where a reported 24 to 33 years gave a significant risk ratio of 7.31; bending, where 21-33 years gave a signficant risk ratio of 12.36, and kneeling where 33 years plus gave a risk ratio of 4.18, cleaning floors on knees gave a risk ratio of 5.28. In each category the controls had substantially higher proportions in the lowest tertile than victims. There was falloff in risk ratio in the highest tertile of victims, plausibly explainable by disability related termination of exposure. None of these are "weak" associations.
Multivariate analysis gave a risk ratio for 21–34 years of bending of 12.91, with a upper limit of 167 (!!!), marginally significant. For 34 years, the risk ratio of 9.81 was not signficant, but upper limit was 125.
Lacking a plausible mechanism for smoking increasing OA, it is plausible that the increase of smoking among controls is caused by pain. The association of BMI with increased OA is mechanistically plausible, but increased BMI caused by pain may account for some of the association. Persons in industrial jobs are frequently selected for being big at the start, another source of uncontrolled confounding with a bias to the null. The cut point of BMI = 25 is equivalent to 155 pounds of weight for a 5'6" tall person, which is not exactly tubby.
Although Manolo Blahnik and shoe fetishists can take some comfort in these data, the Dodger would like to see the cross tabs for BMI and high heeled shoes, and occupational risk factors and high heeled shoes, to rule out confounding.
J Epidemiol Community Health. 2003 Oct;57(10):823-30.
An investigation of risk factors for symptomatic osteoarthritis of the knee in women using a life course approach.
Dawson J, Juszczak E, Thorogood M, Marks SA, Dodd C, Fitzpatrick R.Oxford Centre for Health Care Research and Development (OCHRAD) School of Health and Social Care, Oxford Brookes University, 44 London Road, Oxford OX3 7PD, UK. jdawson@brookes.ac.ukSTUDY
Sunday, May 22, 2005
It's an ill wind - necropsy results for air pollution effects.
A Brazilian study provides an effect level for lung pathology associated with air pollution. The study was co-authored by CA Pope, a lead investigator for associations between air pollution and mortality in the US. The investigators noted that in the high exposure area "PM10 attains annual concentrations ranging from 80 to 100 mcg/m3 (24 h mean) [checked the number i the paper] between 1991 and 1995, a level of pollution that was demonstrated to be associated with increased mortality in Sa˜o Paulo." The EPA NAAQS for PM10 is 50 ug/M3 annual average. The Sao Paulo exposures, which were higher than the EPA limit, were clearly an effect level. A "safe" exposure is an extrapolation factor below the no effect level, which would in turn be an extrapolation factor below the effect level observed here. For setting references doses based on laboratory studies, a 10-fold extrapolation factor would be used for each. Here, even a two-fold extrapolation factor gets us below the EPA 50 ug/M3 limit. Therefore, this study provides clear evidence that the NAAQS is not sufficiently protective.
Lung tissue samples were collected during necropsies of [84] individuals who died due to violent causes...The exposed group was composed of individuals who lived in an area with high mean levels of inhalable particles. Control individuals lived in two cities with economies based on agricultural activities...Information about cigarette smoking and occupational exposure was obtained from family members. ... Lungs collected from the high pollution area presented evidence of morehistopathologic damage in comparison to those from the clean environments.
Morphometric evaluation of the main bronchus was conducted to
determine the volume ratio of submucosal glands. Histopathologic alterations of the bronchioli
were evaluated by scoring the presence of inflammatory reaction, wall thickening, and secretory
hyperplasia. The number of spots of carbon deposition was counted along the regions of
lymphatic drainage (visceral pleura and axial connective tissue around bronchi and blood vessels). These effects were observed even after controlling for individual differences in age, sex, and cigarette smoking levels.
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(CHEST 1998; 113:1312-18)
Respiratory Changes due to Long-term Exposure to Urban Levels of Air Pollution: A Histopathologic Study in Humans
Marcelo B. Souza, MD; Paulo H. N. Saldiva, MD, PhD, FCCP;
C. Arden Pope III, PhD; and Vera Luiza Capelozzi, MD, PhD
Lung tissue samples were collected during necropsies of [84] individuals who died due to violent causes...The exposed group was composed of individuals who lived in an area with high mean levels of inhalable particles. Control individuals lived in two cities with economies based on agricultural activities...Information about cigarette smoking and occupational exposure was obtained from family members. ... Lungs collected from the high pollution area presented evidence of morehistopathologic damage in comparison to those from the clean environments.
Morphometric evaluation of the main bronchus was conducted to
determine the volume ratio of submucosal glands. Histopathologic alterations of the bronchioli
were evaluated by scoring the presence of inflammatory reaction, wall thickening, and secretory
hyperplasia. The number of spots of carbon deposition was counted along the regions of
lymphatic drainage (visceral pleura and axial connective tissue around bronchi and blood vessels). These effects were observed even after controlling for individual differences in age, sex, and cigarette smoking levels.
>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
(CHEST 1998; 113:1312-18)
Respiratory Changes due to Long-term Exposure to Urban Levels of Air Pollution: A Histopathologic Study in Humans
Marcelo B. Souza, MD; Paulo H. N. Saldiva, MD, PhD, FCCP;
C. Arden Pope III, PhD; and Vera Luiza Capelozzi, MD, PhD
Saturday, May 21, 2005
Striking Air Pollution Results
Health effects of inhaled particles are more easily observed among non smokers than smokers, because of lower non-pollution related exposures. This makes Utah a prime venue for study. Papers reviewed below were early data regarding inadequacy of current EPA particulate limits.
Utah Valley residents are predominantly nonsmoking members of the Church of Jesus Christ of Latter-day Saints (Mormons). The area has moderately high average PM10 levels with periods of highly elevated PM10 concentrations due to local emissions being trapped in a stagnant air mass near the valley floor during low-level temperature inversion episodes. [The cited paper doesn't contain the exposure levels; the paper heavily references others which contain these data.] Due to a labor dispute, there was intermittent operation of the single largest pollution source, an old integrated steel mill. Levels of other common pollutants including sulfur dioxide, ozone, and acidic aerosol are relatively low. Studies specific to Utah Valley have observed that elevated PM10 concentrations are associated with: (1) decreased lung function; (2) increased incidence of respiratory symptoms; (3) increased school absenteeism; (4) increased respiratory hospital admissions; and (5) increased mortality, especially respiratory and cardiovascular mortality.
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Toxicology. 1996 Jul 17;111(1-3):149-55.
Adverse health effects of air pollutants in a nonsmoking population.
Pope CA 3rd.
Brigham Young University, Provo, Utah 84602, USA.
Utah Valley residents are predominantly nonsmoking members of the Church of Jesus Christ of Latter-day Saints (Mormons). The area has moderately high average PM10 levels with periods of highly elevated PM10 concentrations due to local emissions being trapped in a stagnant air mass near the valley floor during low-level temperature inversion episodes. [The cited paper doesn't contain the exposure levels; the paper heavily references others which contain these data.] Due to a labor dispute, there was intermittent operation of the single largest pollution source, an old integrated steel mill. Levels of other common pollutants including sulfur dioxide, ozone, and acidic aerosol are relatively low. Studies specific to Utah Valley have observed that elevated PM10 concentrations are associated with: (1) decreased lung function; (2) increased incidence of respiratory symptoms; (3) increased school absenteeism; (4) increased respiratory hospital admissions; and (5) increased mortality, especially respiratory and cardiovascular mortality.
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Toxicology. 1996 Jul 17;111(1-3):149-55.
Adverse health effects of air pollutants in a nonsmoking population.
Pope CA 3rd.
Brigham Young University, Provo, Utah 84602, USA.
Thursday, May 19, 2005
Gasoline Engine Emissions include PM10, supporting IARC Possibly Carcinogenic Rating
Twenty-four properly functioning and six high carbon monoxide emission light-duty gasoline vehicles were emission 3 procedures. All were 1990-1997 model year vehicles tested on both an oxygenated and a nonoxygenated fuel. PM10 emission rates for the properly functioning vehicles using oxygenated fuel averaged 6.1, 3.6, and 12.7 mg/mi for the FTP, UC, and REP05, respectively. The corresponding values for the high emitters were 52, 28, and 24 mg/mi. Use of oxygenated fuel significantly reduces PM10 on the FTP, with all the reduction occurring during the cold start. PM10 was mostly carbonaceous material, 36% of which was classified as organic. Driving cycle had a significant impact on the distribution of the emitted polynuclear aromatic hydrocarbons.
Environ Sci Technol. 2001 Jan 1;35(1):26-32.
In-use light-duty gasoline vehicle particulate matter emissions on three driving cycles.
Cadle SH, Mulawa P, Groblicki P, Laroo C, Ragazzi RA, Nelson K, Gallagher G, Zielinska B.General Motors R&D Center, Warren, Michigan 48090-9055, USA. steven.h.cadle@gm.com
Environ Sci Technol. 2001 Jan 1;35(1):26-32.
In-use light-duty gasoline vehicle particulate matter emissions on three driving cycles.
Cadle SH, Mulawa P, Groblicki P, Laroo C, Ragazzi RA, Nelson K, Gallagher G, Zielinska B.General Motors R&D Center, Warren, Michigan 48090-9055, USA. steven.h.cadle@gm.com
Wednesday, May 18, 2005
An Older Review of Rat to Man extrapolation of fibers
BrooklynDodger warns that this review may have been included in the later review by the germans. It may be that crocidolite and amosite pose a higher unit risk, fiber for fiber than chrysotile in people, although that at best makes chrysotile not as bad as the worst thing in the world.
The excess risk of tumours exposed to asbestos were previously compared with the results of rat inhalation experiments. It could be demonstrated that humans at the workplace suffer from a tumour risk at fibre concentrations which are 300 times lower than those needed in the rat inhalation model to produce the same risk. On comparing the risk of lung cancer in this study with the risk of lung cancer for chrysotile textile workers, it can be concluded, that the risk of lung cancer and mesothelioma from crocidolite and amosite was higher than in the chrysotile textile factory. Carcinogenic response was observed at a fibre concentration 6000 times higher in animal inhalation experiments with crocidolite asbestos (SEM analysis of WHO fibres). As a result of these findings, it has been concluded that inhalation studies in rats are not sufficiently sensitive for the detection of hazards and risks to humans exposed to man-made fibres.
Ann Occup Hyg. 1995 Oct;39(5):715-25.
Airborne fibre concentrations and lung burden compared to the tumour response in rats and humans exposed to asbestos.
Rodelsperger K, Woitowitz HJ.Institute and Outpatient Clinic of Occupational and Social Medicine, Justus-Liebig-University, Giessen, Germany.
The excess risk of tumours exposed to asbestos were previously compared with the results of rat inhalation experiments. It could be demonstrated that humans at the workplace suffer from a tumour risk at fibre concentrations which are 300 times lower than those needed in the rat inhalation model to produce the same risk. On comparing the risk of lung cancer in this study with the risk of lung cancer for chrysotile textile workers, it can be concluded, that the risk of lung cancer and mesothelioma from crocidolite and amosite was higher than in the chrysotile textile factory. Carcinogenic response was observed at a fibre concentration 6000 times higher in animal inhalation experiments with crocidolite asbestos (SEM analysis of WHO fibres). As a result of these findings, it has been concluded that inhalation studies in rats are not sufficiently sensitive for the detection of hazards and risks to humans exposed to man-made fibres.
Ann Occup Hyg. 1995 Oct;39(5):715-25.
Airborne fibre concentrations and lung burden compared to the tumour response in rats and humans exposed to asbestos.
Rodelsperger K, Woitowitz HJ.Institute and Outpatient Clinic of Occupational and Social Medicine, Justus-Liebig-University, Giessen, Germany.
Monday, May 16, 2005
ETS study confirms risks of low levels of particulate exposure to cardiovascular health
BrooklynDodger is not all that interested in environmental tobacco smoke as an environmental or occupational hazard, except as it informs understanding of particulate air pollution and industrially generated airborne particles in the workplace. Tobacco smoke is our best example of the high dose to low dose continuity of risk from direct smoking to ETS as a carcinogenic hazard. This paper demonstrates a mechanism for continuity in risk for cardiac effects. Decreased heart rate variability sounds like a good thing but is considered a bad thing, a risk for heart problems.
The abstract paraphrased: Environmental tobacco smoke (ETS) has been associated with cardiovascular mortality. Reduced cardiac autonomic function, as measured by heart rate variability (HRV), has been associated with cardiac vulnerability and may represent an important pathophysiologic mechanism linking ETS and risk of cardiac mortality. ...ETS exposure in a commercial airport with changes in HRV in 16 adult nonsmokers..Participants alternated 2 hr in nonsmoking and smoking areas. ... During exposure periods, we observed an average decrement of approximately 12% in the standard deviation of all normal-to-normal heart beat intervals (an estimate of overall HRV). ... Altered cardiac autonomic function, assessed by decrements in HRV, is associated with acute exposure to ETS and may be part of the pathophysiologic mechanisms linking ETS exposure and increased cardiac vulnerability.
The RSP levels in µg/m3 were 24.74 in non smoking areas [the Dodger would not have permitted 4 significant figures if he were the reviewer or editor, nor allowed a table without a measure of variability, and would likely have insisted on a geometric mean and GSD] and 77.97 in the smoking area. The non-smoking area thus had exposures above the EPA annual averate permitted level for PM2.5; this high level would make it more difficult to see the effect if it were there.
Thus, cardiac effects of tobacco smoke may no longer be attributed solely to CO or nicotine.
EHP is available in full text via internet.
>>>>>>>>>>>>>>>>>>>>>>>>
Environ Health Perspect 109:711-716 (2001).
Acute Exposure to Environmental Tobacco Smoke and Heart Rate Variability
C. Arden Pope, III,1 Delbert J. Eatough,1 Diane R. Gold,2 Yanbo Pang,1 Karen R. Nielsen,3 Prema Nath,4 Richard L. Verrier,5 and Richard E. Kanner6
1Department of Chemistry & Biochemistry and Department of Economics, Brigham Young University, Provo, Utah; 2Channing Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA; 3Cardiovascular Genetic Research Clinic, University of Utah School of Medicine, Salt Lake City, Utah, USA; 4University of Utah Hospital and Clinics, Salt Lake City, Utah, USA; 5Institute for Prevention of Cardiovascular Disease, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA; 6Division of Respiratory, Critical Care and Occupational Medicine, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City, Utah, USA
The abstract paraphrased: Environmental tobacco smoke (ETS) has been associated with cardiovascular mortality. Reduced cardiac autonomic function, as measured by heart rate variability (HRV), has been associated with cardiac vulnerability and may represent an important pathophysiologic mechanism linking ETS and risk of cardiac mortality. ...ETS exposure in a commercial airport with changes in HRV in 16 adult nonsmokers..Participants alternated 2 hr in nonsmoking and smoking areas. ... During exposure periods, we observed an average decrement of approximately 12% in the standard deviation of all normal-to-normal heart beat intervals (an estimate of overall HRV). ... Altered cardiac autonomic function, assessed by decrements in HRV, is associated with acute exposure to ETS and may be part of the pathophysiologic mechanisms linking ETS exposure and increased cardiac vulnerability.
The RSP levels in µg/m3 were 24.74 in non smoking areas [the Dodger would not have permitted 4 significant figures if he were the reviewer or editor, nor allowed a table without a measure of variability, and would likely have insisted on a geometric mean and GSD] and 77.97 in the smoking area. The non-smoking area thus had exposures above the EPA annual averate permitted level for PM2.5; this high level would make it more difficult to see the effect if it were there.
Thus, cardiac effects of tobacco smoke may no longer be attributed solely to CO or nicotine.
EHP is available in full text via internet.
>>>>>>>>>>>>>>>>>>>>>>>>
Environ Health Perspect 109:711-716 (2001).
Acute Exposure to Environmental Tobacco Smoke and Heart Rate Variability
C. Arden Pope, III,1 Delbert J. Eatough,1 Diane R. Gold,2 Yanbo Pang,1 Karen R. Nielsen,3 Prema Nath,4 Richard L. Verrier,5 and Richard E. Kanner6
1Department of Chemistry & Biochemistry and Department of Economics, Brigham Young University, Provo, Utah; 2Channing Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA; 3Cardiovascular Genetic Research Clinic, University of Utah School of Medicine, Salt Lake City, Utah, USA; 4University of Utah Hospital and Clinics, Salt Lake City, Utah, USA; 5Institute for Prevention of Cardiovascular Disease, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA; 6Division of Respiratory, Critical Care and Occupational Medicine, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City, Utah, USA
Sunday, May 15, 2005
Diesel Particulate Matter v. Gasoline Particulate
BrooklynDodger opines that toxicity of vehicle exhaust emissions cruxes energy policy. Transition to light vehicle diesels would dramatically boost CAFE, but is there a health cost? Diesel Particulate Matter is a bad boy, but maybe in comparison only because hazards of gasoline engine emissions have been swept under the rug. Regarding CNG engine emissions, both industry and the environmental community have united behind don't ask, don't tell, don't persue.
Now comes a study from NIOSH Morgantown, which operates across the street from DOE laboratories [courtesy Robert Byrd.] This informs truck driver lung cancer studies; truckers are exposed to highway particulate, which includes both gasoline and diesel emissions. Gasoline emissions are IARC 2B, vs. diesel which is a 2B. These lab data show extracts of the particles are roughly equitoxic; it would be nice to compare the full particle exposure to that of CNG particles.
Acetone extracts of engine exhaust particulate matter (PM) and of vapor-phase semi-volatile organic compounds (SVOCs) collected from diesel and from gasoline engines were assayed for in vitro genotoxic activities. Gasoline and diesel PM were comparably positive mutagens on a mass of PM extract basis with diesel higher on a mileage basis; gasoline SVOC was more active than diesel on an extracted-mass basis, with diesel SVOC more active on a mileage basis. For chromosomal damage diesel PM expressed about one-tenth that of gasoline PM on a mass of extract basis, but was comparably active on a mileage basis; diesel SVOC was inactive. For DNA damage gasoline PM was positive while diesel PM was active at the higher doses; gasoline SVOC was active with toxicity preventing measurement at high doses, while diesel SVOC was inactive at all but the highest dose.
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J Environ Monit. 2005 Jan;7(1):60-6. Epub 2004 Dec 8.
In vitro genotoxicity of exhaust emissions of diesel and gasoline engine vehicles operated on a unified driving cycle.
Liu YQ, Keane M, Ensell M, Miller W, Kashon M, Ong TM, Mauderly J, Lawson D, Gautam M, Zielinska B, Whitney K, Eberhardt J, Wallace W.National Institute for Occupational Safety and Health, 1095 Willowdale Rd., Morgantown, WV 26505, USA.
Now comes a study from NIOSH Morgantown, which operates across the street from DOE laboratories [courtesy Robert Byrd.] This informs truck driver lung cancer studies; truckers are exposed to highway particulate, which includes both gasoline and diesel emissions. Gasoline emissions are IARC 2B, vs. diesel which is a 2B. These lab data show extracts of the particles are roughly equitoxic; it would be nice to compare the full particle exposure to that of CNG particles.
Acetone extracts of engine exhaust particulate matter (PM) and of vapor-phase semi-volatile organic compounds (SVOCs) collected from diesel and from gasoline engines were assayed for in vitro genotoxic activities. Gasoline and diesel PM were comparably positive mutagens on a mass of PM extract basis with diesel higher on a mileage basis; gasoline SVOC was more active than diesel on an extracted-mass basis, with diesel SVOC more active on a mileage basis. For chromosomal damage diesel PM expressed about one-tenth that of gasoline PM on a mass of extract basis, but was comparably active on a mileage basis; diesel SVOC was inactive. For DNA damage gasoline PM was positive while diesel PM was active at the higher doses; gasoline SVOC was active with toxicity preventing measurement at high doses, while diesel SVOC was inactive at all but the highest dose.
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J Environ Monit. 2005 Jan;7(1):60-6. Epub 2004 Dec 8.
In vitro genotoxicity of exhaust emissions of diesel and gasoline engine vehicles operated on a unified driving cycle.
Liu YQ, Keane M, Ensell M, Miller W, Kashon M, Ong TM, Mauderly J, Lawson D, Gautam M, Zielinska B, Whitney K, Eberhardt J, Wallace W.National Institute for Occupational Safety and Health, 1095 Willowdale Rd., Morgantown, WV 26505, USA.
Saturday, May 14, 2005
Is there something special about silica?
BrooklynDodger grew up when we wondered why asbestos caused fibrosis and cancer, but silica only fibrosis, and other dusts were non-toxic. We knew why tobacco smoke was carcinogenic [PAH's absorbed on carbon particles] even those tobacco smoke was not carcinogenic in rats by inhalation.
Now, silica is a Class 1 human carcinogen, based on epidemiology and bioassay data. Tobacco smoke has been shown carcinogenic in the rat [but not the mouse], but about 50 fold less potent than silica. Many other dusts, including the "non-carcinogenic" control titanium dioxide, are carcinogenic in the rat. [The strongest epidemiological study of titanium dioxide exposed workers is inadequate to measure carcinogenicity of titanium dioxide, and is not as null as the authors content.] Carbon black and diesel particulate matter are similarly potent in the rat, and similarly more potent than tobacco smoke.
Back in the day, the theory of silica fibrosis was that the silica particles killed pulmonary macrophages, leading to fibrosis. BrooklynDodger will look for a bibliography on in vitro and in vivo comparative toxicity to macrophage studies. Comparing behavior of various dusts in various systems is valuable to probe whether all particles should be treated similarly.
The paper below involves techniques the Dodger thinks appeared after the Dodger left the lab. Paraphrasing the abstract, ... the alveolar macrophage (AM) is considered key to the effects of silica on lung pathology...evidence suggests an increase in antigen presenting cell (APC) activity as a contributing factor to this process, as well as potential roles for both AM and interstitial macrophages (IM) in silicosis. ...Mice were exposed intranasally...Following intranasal instillation of silica, a significant increase in the APC activity of AM was observed, as well as a significant increase in a subset of IM expressing classic APC markers...... bone marrow-derived macrophages (BMDM)... in the in vitro APC assay demonstrated a significant increase in APC activity following silica exposure, but not following exposure to saline or a control particle (TiO2). ... These studies suggest a specific mechanism, macrophage subset activation, by which crystalline silica exposure results in chronic pulmonary inflammation and, eventually, fibrosis.
The problem with this paper is the titanium dioxide particle control. The investigators tell us the silica particles are 1.5-2 microns, and the "Treatments included saline alone, 1 mg crystalline silica in saline, or 0.5 mg TiO2 (as a control particle) in saline." There were some effects, not statistically significant from titanium dioxide [given at half the dose], and particle size is a big deal for titanium dioxide and the that's not given. So the study is inadequate to draw strong, if any conclusions about the contrast between silica and titanium dioxide. So, we still don't know if there is something special about silica.
Why the referees and editors let this get by, the Dodger is mystified. TAP is a top of the line journal.
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Toxicology and Applied Pharmacology Volume 205, Issue 2 , 1 June 2005, Pages 168-176
Increase in a distinct pulmonary macrophage subset possessing an antigen-presenting cell phenotype and in vitro APC activity following silica exposure
Christopher T. Migliaccio, , Raymond F. Hamilton, Jr. and Andrij Holian Center for Environmental Health Sciences, Biomedical and Pharmaceutical Sciences, University of Montana, 155 Skaggs Building, Missoula, MT 59812, USA Received 17 August 2004; accepted 2 November 2004. Available online 21 January 2005.
Now, silica is a Class 1 human carcinogen, based on epidemiology and bioassay data. Tobacco smoke has been shown carcinogenic in the rat [but not the mouse], but about 50 fold less potent than silica. Many other dusts, including the "non-carcinogenic" control titanium dioxide, are carcinogenic in the rat. [The strongest epidemiological study of titanium dioxide exposed workers is inadequate to measure carcinogenicity of titanium dioxide, and is not as null as the authors content.] Carbon black and diesel particulate matter are similarly potent in the rat, and similarly more potent than tobacco smoke.
Back in the day, the theory of silica fibrosis was that the silica particles killed pulmonary macrophages, leading to fibrosis. BrooklynDodger will look for a bibliography on in vitro and in vivo comparative toxicity to macrophage studies. Comparing behavior of various dusts in various systems is valuable to probe whether all particles should be treated similarly.
The paper below involves techniques the Dodger thinks appeared after the Dodger left the lab. Paraphrasing the abstract, ... the alveolar macrophage (AM) is considered key to the effects of silica on lung pathology...evidence suggests an increase in antigen presenting cell (APC) activity as a contributing factor to this process, as well as potential roles for both AM and interstitial macrophages (IM) in silicosis. ...Mice were exposed intranasally...Following intranasal instillation of silica, a significant increase in the APC activity of AM was observed, as well as a significant increase in a subset of IM expressing classic APC markers...... bone marrow-derived macrophages (BMDM)... in the in vitro APC assay demonstrated a significant increase in APC activity following silica exposure, but not following exposure to saline or a control particle (TiO2). ... These studies suggest a specific mechanism, macrophage subset activation, by which crystalline silica exposure results in chronic pulmonary inflammation and, eventually, fibrosis.
The problem with this paper is the titanium dioxide particle control. The investigators tell us the silica particles are 1.5-2 microns, and the "Treatments included saline alone, 1 mg crystalline silica in saline, or 0.5 mg TiO2 (as a control particle) in saline." There were some effects, not statistically significant from titanium dioxide [given at half the dose], and particle size is a big deal for titanium dioxide and the that's not given. So the study is inadequate to draw strong, if any conclusions about the contrast between silica and titanium dioxide. So, we still don't know if there is something special about silica.
Why the referees and editors let this get by, the Dodger is mystified. TAP is a top of the line journal.
>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
Toxicology and Applied Pharmacology Volume 205, Issue 2 , 1 June 2005, Pages 168-176
Increase in a distinct pulmonary macrophage subset possessing an antigen-presenting cell phenotype and in vitro APC activity following silica exposure
Christopher T. Migliaccio, , Raymond F. Hamilton, Jr. and Andrij Holian Center for Environmental Health Sciences, Biomedical and Pharmaceutical Sciences, University of Montana, 155 Skaggs Building, Missoula, MT 59812, USA Received 17 August 2004; accepted 2 November 2004. Available online 21 January 2005.
Wednesday, May 11, 2005
Asbestos Effect Levels in Lab Studies
German colleagues provide a revealing review connecting laboratory studies of carcinogenicity of inhaled asbestos to those in people. The Houdini risk assessment community argues rats are too sensitive to particulate inhalation, since tumors [from particulates including asbestos] appear in rats, but not in mice or hamsters.
[Notably, solvent vapors cause lung tumors in mice but not rats under bioassay conditions. Therefore, the Houdinist community argues that people are like rats when it comes to vapors, and mice when it comes to particles.]
Rarely mentioned is the effect level in those studies, which is in the range of 1000 fibers/cc. BrooklynDodger opines that relative toxicity of alternative materials can be ballparked by comparing effect levels in laboratory studies, but that relative toxicity should be applied to effect levels of asbestos in people, not quantitated back from the lab tests in rats.
The investigators reviewed published data on the carcinogenicity of asbestos fibres in laboratory studies to compare effect levels to studies of exposure to man-made vitreous fibres (MMVF). [Now called synthetic mineral fibers, since some are likely made by women.]Various dust samples of chrysotile, crocidolite, and amosite were used as reference materials in studies with experimental animals. Data from biopersistence studies show that focusing only on fibres longer than 20 microm and using weighted half-time for a characterization of risk may be misleading. Inhalation experiments with rats need fibre exposure concentrations over 100 times higher to match the lung cancer risk of asbestos workers, and about 1,000 times higher to reach the same mesothelioma risk. Also, the striking difference between the low lung burden of amphibole fibres of asbestos workers with mesothelioma and the more than 1,000 times higher lung burden of rats with a low mesothelioma risk demonstrates the low sensitivity of the inhalation test model for the carcinogenic potency even of crocidolite fibres. The rat inhalation model is also not sensitive enough to predict the cancer risk of other fibre types for humans.
Int Arch Occup Environ Health. 2000 Jun;73 Suppl:S53-9.
Asbestos as reference material for fibre-induced cancer.
Muhle H, Pott F.Fraunhofer Institute of Toxicology and Aerosol Research, Hannover, Germany. muhle@ita.fhg.de
[Notably, solvent vapors cause lung tumors in mice but not rats under bioassay conditions. Therefore, the Houdinist community argues that people are like rats when it comes to vapors, and mice when it comes to particles.]
Rarely mentioned is the effect level in those studies, which is in the range of 1000 fibers/cc. BrooklynDodger opines that relative toxicity of alternative materials can be ballparked by comparing effect levels in laboratory studies, but that relative toxicity should be applied to effect levels of asbestos in people, not quantitated back from the lab tests in rats.
The investigators reviewed published data on the carcinogenicity of asbestos fibres in laboratory studies to compare effect levels to studies of exposure to man-made vitreous fibres (MMVF). [Now called synthetic mineral fibers, since some are likely made by women.]Various dust samples of chrysotile, crocidolite, and amosite were used as reference materials in studies with experimental animals. Data from biopersistence studies show that focusing only on fibres longer than 20 microm and using weighted half-time for a characterization of risk may be misleading. Inhalation experiments with rats need fibre exposure concentrations over 100 times higher to match the lung cancer risk of asbestos workers, and about 1,000 times higher to reach the same mesothelioma risk. Also, the striking difference between the low lung burden of amphibole fibres of asbestos workers with mesothelioma and the more than 1,000 times higher lung burden of rats with a low mesothelioma risk demonstrates the low sensitivity of the inhalation test model for the carcinogenic potency even of crocidolite fibres. The rat inhalation model is also not sensitive enough to predict the cancer risk of other fibre types for humans.
Int Arch Occup Environ Health. 2000 Jun;73 Suppl:S53-9.
Asbestos as reference material for fibre-induced cancer.
Muhle H, Pott F.Fraunhofer Institute of Toxicology and Aerosol Research, Hannover, Germany. muhle@ita.fhg.de
Tuesday, May 10, 2005
Brake Shoe Asbestos Exposures
BrooklynDodger assumes this study was funded to provide data for defense of asbestos liability suits. The Dodger reminds the gentle reader that OSHA estimates a near doubling of lung cancer risk at exposure at the 0.1 fiber/cc limit over a working lifetime. BrooklynDodger opines that these exposure levels are physiologically signficant although the effects may not be epidemiologically signficant.
Evaluation of fibers and total particulate generated during the servicing of drum brakes on motor vehicles as well as during the resurfacing (arcing) of brake shoes was conducted. Phase 1 estimated the release of asbestos fibers and total particulate during brake inspection and replacement of light-duty vehicle rear drum brakes at an auto/truck repair facility. One rear wheel from each vehicle was serviced using compressed air to remove dust while the second rear wheel was serviced without compressed air. Fiber levels without compressed air ranged from 0.05 to 0.2 f/cc. Fiber counts when using compressed air averaged from 0.05 to 0.9 f/cc. Results from real-time aerosol monitoring indicated elevated dust levels for about 15 minutes after blow out. With shop doors open, dust levels increased to 5.0 mg/m3 at blow out and returned to 0.08 mg/m3 within two minutes. When the shop doors were closed, the dust levels reached 13.5 mg/m3 at blow out and decreased to 1.68 mg/m3 within one minute and to background within 14 minutes.
For grinding operations conducted under conditions simulating a workplace, a mean of 0.19 f/cc was determined. Dust levels averaged 0.25 mg/m3 +/- 0.05. Considered on a time weighted average basis, should not exceed currently acceptable workplace standards whether or not the worker uses compressed air, nor during the arc grinding process when arcing is conducted in accord with the design of the equipment.
Appl Occup Environ Hyg. 2001 Dec;16(12):1139-46.
Characterization of vehicular brake service personnel exposure to airborne asbestos and particulate.
Weir FW, Tolar G, Meraz LB.Francis W. Weir, Ph.D, Inc, Houston, Texas, USA.
Evaluation of fibers and total particulate generated during the servicing of drum brakes on motor vehicles as well as during the resurfacing (arcing) of brake shoes was conducted. Phase 1 estimated the release of asbestos fibers and total particulate during brake inspection and replacement of light-duty vehicle rear drum brakes at an auto/truck repair facility. One rear wheel from each vehicle was serviced using compressed air to remove dust while the second rear wheel was serviced without compressed air. Fiber levels without compressed air ranged from 0.05 to 0.2 f/cc. Fiber counts when using compressed air averaged from 0.05 to 0.9 f/cc. Results from real-time aerosol monitoring indicated elevated dust levels for about 15 minutes after blow out. With shop doors open, dust levels increased to 5.0 mg/m3 at blow out and returned to 0.08 mg/m3 within two minutes. When the shop doors were closed, the dust levels reached 13.5 mg/m3 at blow out and decreased to 1.68 mg/m3 within one minute and to background within 14 minutes.
For grinding operations conducted under conditions simulating a workplace, a mean of 0.19 f/cc was determined. Dust levels averaged 0.25 mg/m3 +/- 0.05. Considered on a time weighted average basis, should not exceed currently acceptable workplace standards whether or not the worker uses compressed air, nor during the arc grinding process when arcing is conducted in accord with the design of the equipment.
Appl Occup Environ Hyg. 2001 Dec;16(12):1139-46.
Characterization of vehicular brake service personnel exposure to airborne asbestos and particulate.
Weir FW, Tolar G, Meraz LB.Francis W. Weir, Ph.D, Inc, Houston, Texas, USA.
Monday, May 09, 2005
Stuctures v. Fibers in Brake Shoe Operations
Do brake repair operations entail epidemiologically meaningful asbestos exposures? Epidemiologically meaningful means exposure high enough to yield 3 lung cancers in 1000 exposed workers, approximately an SMR of 1.5. Physiologically meaningful exposures might be lower, an exposure increasing the rate of pleural placques on x-ray with a 20 year lag from accumulated fiber-years or structure years of exposure.
OSHA's risk assessment, based on human data, projects an attributable lung cancer rate of 6 per 1000 at the current PEL of 0.1 fibers/cc, which is a 45 year exposure of 4.5 fiber-years. BrooklynDodger guesses that 0.1 fiber/cc is about the limit of quantitation for fibers in an environment clean of other particulate. Below that, exposure would have to be measured with "structure" on TEM.
These investigators are based in Tyler, Texas, ground zero for one of the key factory studies of yesteryear. They report that at one point Chrysotile comprised 40-50% of the composition of brake linings. Unused brake linings or brake shoes with attached linings from four different sources were gently rinsed with prefiltered water that was then collected on filters for analysis by Analytical Transmission Electron Microscope. Large numbers of chrysotile asbestos containing structures, the majority of respirable size, were present in each sample. The investigators concluded that any manipulation of new asbestos containing brake components would be expected to yield free dust containing chrysotile asbestos of respirable size. That the vast majority of these fibers and particulates would not be counted as regulated fibers.
The full paper has lots of interesting pictures.
BrooklynDodger suspects the friable asbestos in the boxes is actually fallout dust from the factory making the friction product. It would be unlikely that bouncing around in the box would cause wear enough to generate the dust. The best way to protect the auto mechanics would be to reduce dust in the manufacturing plant [where ever it is, likely not in the US] and clean the product before packing.
>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
Am J Ind Med. 2004 Dec;46(6):545-53.
Evaluation of the size and type of free particulates collected from unused asbestos-containing brake components as related to potential for respirability.
Atkinson MA, O'sullivan M, Zuber S, Dodson RF.
The University of Texas Health Center at Tyler, Tyler, Texas 75708, USA.
OSHA's risk assessment, based on human data, projects an attributable lung cancer rate of 6 per 1000 at the current PEL of 0.1 fibers/cc, which is a 45 year exposure of 4.5 fiber-years. BrooklynDodger guesses that 0.1 fiber/cc is about the limit of quantitation for fibers in an environment clean of other particulate. Below that, exposure would have to be measured with "structure" on TEM.
These investigators are based in Tyler, Texas, ground zero for one of the key factory studies of yesteryear. They report that at one point Chrysotile comprised 40-50% of the composition of brake linings. Unused brake linings or brake shoes with attached linings from four different sources were gently rinsed with prefiltered water that was then collected on filters for analysis by Analytical Transmission Electron Microscope. Large numbers of chrysotile asbestos containing structures, the majority of respirable size, were present in each sample. The investigators concluded that any manipulation of new asbestos containing brake components would be expected to yield free dust containing chrysotile asbestos of respirable size. That the vast majority of these fibers and particulates would not be counted as regulated fibers.
The full paper has lots of interesting pictures.
BrooklynDodger suspects the friable asbestos in the boxes is actually fallout dust from the factory making the friction product. It would be unlikely that bouncing around in the box would cause wear enough to generate the dust. The best way to protect the auto mechanics would be to reduce dust in the manufacturing plant [where ever it is, likely not in the US] and clean the product before packing.
>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
Am J Ind Med. 2004 Dec;46(6):545-53.
Evaluation of the size and type of free particulates collected from unused asbestos-containing brake components as related to potential for respirability.
Atkinson MA, O'sullivan M, Zuber S, Dodson RF.
The University of Texas Health Center at Tyler, Tyler, Texas 75708, USA.
Sunday, May 08, 2005
More on Particles and Life
BrooklynDodger finds another paper about particulate pollution and overall mortality, this authored by a top research group from Johns Hopkins. This continues the Dodger’s quest to apply the community data in the occupational environment. Observed increases in overall mortality are in the range of 0.2% for each increase of 10 ug/M3. The variations observed were mostly within the 150 ug/m3 daily and 65 ug/M3 annual average limit for PM10.
The Dodger paraphrases the abstract as follows: The National Morbidity and Mortality Air Pollution Study includes data for 100 US cities, For the period 1987–2000, at the national level, a 10-µg/m3 increase in particulate matter less than 10 µm in aerodynamic diameter [PM10, roughly equivalent to the industrial hygienist’s Total Particulate] at a 1-day lag was associated with 0.15%, 0.14%, 0.36%, and 0.14% increases in mortality for winter, spring, summer, and fall, respectively. Analysis by geographic region found a strong seasonal pattern in the Northeast (with a peak in summer) and little seasonal variation in the southern regions of the country.
Is this 0.2% in total mortality a big number or a little number? Given 2,500,000 deaths per year [detail below], this fraction percent is 5000. The Dodger can’t figure out how to estimate deaths per year, but at least this gives a lives prolonged, per 10 ug/M3 reduction. The Dodger remembers that each death takes with it about 10 years of future life.
From NCHS:
Deaths/Mortality
(Data are for U.S. in 2002)
Number of deaths: 2,443,387
Death rate: 845.3 deaths per 100,000 population
Life expectancy: 77.3 years
Number of deaths for leading causes of death:
Heart disease: 696,947
Cancer: 557,271
Stroke: 162,672
Chronic lower respiratory diseases: 124,816
Accidents (unintentional injuries): 106,742
Diabetes: 73,249
Influenza/Pneumonia: 65,681
Alzheimer's disease: 58,866
Nephritis, nephrotic syndrome, and nephrosis: 40,974
Septicemia: 33,865
Source: Deaths: Final Data for 2002
>>>>>>>>>>>>>>>>>>>>>>>>>>
American Journal of Epidemiology 2005 161(6):585-594;
Seasonal Analyses of Air Pollution and Mortality in 100 US Cities
Roger D. Peng1, Francesca Dominici1, Roberto Pastor-Barriuso2, Scott L. Zeger1 and Jonathan M. Samet3
1 Department of Biostatistics, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD2 Epidemiology and Biostatistics Section, National Center for Epidemiology, Carlos III Institute of Health, Madrid, Spain3 Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD
Correspondence to Dr. Roger D. Peng, Department of Biostatistics, Johns Hopkins Bloomberg School of Public Health, 615 North Wolfe Street, Baltimore, MD 21205 (e-mail: rpeng@jhsph.edu
The Dodger paraphrases the abstract as follows: The National Morbidity and Mortality Air Pollution Study includes data for 100 US cities, For the period 1987–2000, at the national level, a 10-µg/m3 increase in particulate matter less than 10 µm in aerodynamic diameter [PM10, roughly equivalent to the industrial hygienist’s Total Particulate] at a 1-day lag was associated with 0.15%, 0.14%, 0.36%, and 0.14% increases in mortality for winter, spring, summer, and fall, respectively. Analysis by geographic region found a strong seasonal pattern in the Northeast (with a peak in summer) and little seasonal variation in the southern regions of the country.
Is this 0.2% in total mortality a big number or a little number? Given 2,500,000 deaths per year [detail below], this fraction percent is 5000. The Dodger can’t figure out how to estimate deaths per year, but at least this gives a lives prolonged, per 10 ug/M3 reduction. The Dodger remembers that each death takes with it about 10 years of future life.
From NCHS:
Deaths/Mortality
(Data are for U.S. in 2002)
Number of deaths: 2,443,387
Death rate: 845.3 deaths per 100,000 population
Life expectancy: 77.3 years
Number of deaths for leading causes of death:
Heart disease: 696,947
Cancer: 557,271
Stroke: 162,672
Chronic lower respiratory diseases: 124,816
Accidents (unintentional injuries): 106,742
Diabetes: 73,249
Influenza/Pneumonia: 65,681
Alzheimer's disease: 58,866
Nephritis, nephrotic syndrome, and nephrosis: 40,974
Septicemia: 33,865
Source: Deaths: Final Data for 2002
>>>>>>>>>>>>>>>>>>>>>>>>>>
American Journal of Epidemiology 2005 161(6):585-594;
Seasonal Analyses of Air Pollution and Mortality in 100 US Cities
Roger D. Peng1, Francesca Dominici1, Roberto Pastor-Barriuso2, Scott L. Zeger1 and Jonathan M. Samet3
1 Department of Biostatistics, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD2 Epidemiology and Biostatistics Section, National Center for Epidemiology, Carlos III Institute of Health, Madrid, Spain3 Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD
Correspondence to Dr. Roger D. Peng, Department of Biostatistics, Johns Hopkins Bloomberg School of Public Health, 615 North Wolfe Street, Baltimore, MD 21205 (e-mail: rpeng@jhsph.edu
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