There's been discussion of monitoring of workers employed for restoration in the hurricane area, and particularly water intruded buildings in NOLA. This is a great opportunity, given public funding of much of this work and public interest in all of it.
The most general occupational illness concerns would be inhalation hazards on small construction, demolition or remodeling sites, present whether in storm damaged areas or not. Most important measurements would be particulate not otherwise classified. Inhalable particulate [IOM sampler or open faced cassette] samples should be collected as well as conventional samples or real time aerosol monitoring. There are no evaluation criteria for inhalable [particles larger than 10 microns]. Evaluation criteria for PM10 [OSHA total] and PM 2.5 [OSHA respirable] should be EPA NAAQS particulate standards.
What about biomass hazards. There's a decent literature on agricultural exposures. Whether it's manure on a pig farm, or slude in a NOLA house, the same principles apply. The mold literature applies, sewage treatment workers, and other waste workers.
The paper abstracted below suggests some environmental measurements which could be made, and some clinical measures of effect which might be observed.
The introductory section of the paper notes:
Adverse health effects in workers involved in the
household waste recycling industry were first described
at a refuse plant in Denmark performing manual
sorting of industrial and household waste.1 Initial symptoms
of nose and eye irritation progressed to cases of organic dust
toxic syndrome (ODTS), bronchial asthma, and chronic bronchitis
in nine of 15 workers during the first year of work, presumably
because of bioaerosol exposure from the waste. Some
case reports also exist of allergic reactions such as hypersensitive
pneumonitis after excessively high fungal spore exposure
from wood chips and residential composting.2 3 The underlying
mechanisms causing the reported health effects are still
unclear, but there is increasing evidence that the respiratory
symptoms caused by bioaerosol exposure are mainly of an
non-allergic inflammatory nature.
BrooklynDodger is going to have to look up beta (1-3) glucans. Right now the Dodger guesses these are something like endotoxin(s).
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Occup Environ Med. 2003 Jun;60(6):444-50. Related Articles, Links
Upper airway inflammation in waste handlers exposed to bioaerosols.
Heldal KK, Halstensen AS, Thorn J, Djupesland P, Wouters I, Eduard W, Halstensen TS.
National Institute of Occupational Health, Oslo, Norway. kari.heldal@stami.no
AIMS: To examine work associated upper airway inflammation in 31 waste handlers, and to correlate these findings with personally monitored exposure to different bioaerosol components. METHODS: Cell differentials, interleukin 8 (IL-8), myeloperoxidase (MPO), and eosinophilic cationic protein (ECP) were examined in NAL (nasal lavage), and swelling of the nasal mucosa was determined by acoustic rhinometry before work start on Monday and the following Thursday. Bioaerosol exposure was determined by personal full shift exposure measurements on Monday, Tuesday, and Wednesday and analysed for total bacteria, fungal spores, endotoxin, and beta(1-->3)-glucans. RESULTS: The increased percentage of neutrophils from Monday (28%) to Thursday (46%) correlated with increases in ECP (r(S) = 0.71, p < p =" 0.07).">3)-glucans (range 3-217 ng/m(3)), respectively (r(S) = 0.47-0.54, p <>3)-glucan exposure (r(S) = 0.58-0.59, p <>3)-glucans during waste handling induced upper airway inflammation dominated by neutrophil infiltration and swelling of the nasal mucosa.
Monday, October 31, 2005
Sunday, October 30, 2005
Popcorn Workers Lung (I) - is it just butter flavoring?)
Popcorn packers lung (PPL) illustrates the strength and some weaknesses of the current incarnation of NIOSH. [This post got out of hand with searching for background, and will tail off at the end. The Dodger will use the "least postable unit" approach to fill up a whole week's traffic.]
The strength of NIOSH is ability to respond to reports with combined occupational medicine, epidemiology, industrial hygiene [exposure characterization] and toxicology resources. The weakness is how long it takes.
The main point here is what should practitioners do to respond to clusters of occupational respiratory disease when they first emerge? The story parallels outbreaks of hypersensitivity pneumonitis in metal machining plants, lifeguard lung, legionaires disease, and even the post office anthrax experience.
Recently, victims at the index plant won judgements against International Flavors and Fragrances, for 10's of millions of dollars for devastating lung disease. Accounts of litigation can be found at http://www.butterflavoringlunginjury.com/
BrooklynDodger started this post noting the JOEH paper on characterization of exposure in the most recent issue, late 2005. The Dodger thought, how long has this been going on, and how long has the OH community been ignorant of the exposure levels? For interest, NIOSH reported
"Diacetyl, the predominant ketone in the plant, was present in
concentrations ranging from below detectable limits to 98 parts per million
parts air by volume (ppm), with a mean of 8.1 ppm (standard deviation 18.5 ppm).
The average ketone concentrations were highest in the microwave mixing room
where the 10 area samples had a mean diacetyl concentration of 37.8 ppm (SD 27.6
ppm)"
[The Dodger faults the authors for reporting, and the reviewers and editors for permitting them to report, arithmetic mean values rather than medians [easy to do], geometric means, or a mean value back calculated from the geometric mean and observed variance. The mean is less stable and suggests a higher exposure level over the population, thereby suggesting a lower unit risk.]
However, these data were reported in the NEJM paper in 2002.
An MMWR report appeared in April 2002, not much in advance of NEJM. The MMWR did report the geometric mean, which was reported as "The geometric mean air concentration of diacetyl was 18 parts per million parts air (ppm) in the room where the mixing tank was located, 1.3 ppm in the microwave-packaging area, and 0.02 ppm in other areas of the plant." [For epidemiologists, the Dodger notes that the geometric mean was 1/2 the arithmetic mean.]
http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5116a2.htm
Thus, the JOEH publication is an echo of previous information, either a product of "least publishable unit" publication or a slow editorial process at the journal.
[to be continued]
BrooklynDodger sympathizes with the team, especially the IH folks. Here's a devastating outbreak of disease. The most prominent chemical exposure is a food additive. Probably there's no toxicity data for this chemical, if there is it's probably feeding. [BrooklynDodger is going to work on this in the tox post]. It probably isn't that irritating and it does smell good. 100 ppm is a lot of organic vapor these days, but IH's think of 100 ppm as a TLV for a not specially toxic solvent.
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J Occup Environ Hyg. 2005 Mar;2(3):169-78.
Characterization of respiratory exposures at a microwave popcorn plant with cases of bronchiolitis obliterans.
Kullman G, Boylstein R, Jones W, Piacitelli C, Pendergrass S, Kreiss K.
National Institute for Occupational Safety and Health (NIOSH), Morgantown, West Virginia 26505, USA. gjk1@cdc.gov
Eight former workers from a microwave popcorn packaging plant were reported to have severe obstructive lung disease consistent with bronchiolitis obliterans. Investigations into respiratory exposures at this plant were done during August through November of 2000. ... Workers in the microwave production areas of the plant were exposed to particulates and a range of organic vapors from flavorings. The particles were comprised largely of salt and oil/grease particles. Respirable dust concentrations (area plus personal) in the microwave mixer job category, the highest job exposure category in the plant, ranged from 0.13 milligrams per cubic meter of air (mg/m3) to a high of 0.77 mg/m3. ...The predominant compounds identified in the microwave mixing room included the ketones diacetyl, methyl ethyl ketone, acetoin, and 2-nonanone, and acetic acid.
Diacetyl, the predominant ketone in the plant, was present in concentrations ranging from below detectable limits to 98 parts per million parts air by volume (ppm), with a mean of 8.1 ppm (standard deviation 18.5 ppm). The average ketone concentrations were highest in the microwave mixing room where the 10 area samples had a mean diacetyl concentration of 37.8 ppm (SD 27.6 ppm) and a mean acetoin concentration of 3.9 ppm (SD 4.3 ppm). These data show that workers involved in microwave popcorn packaging can be exposed to a complex mixture of VOCs from flavoring ingredients; animal studies show that diacetyl can cause airway epithelial injury, although the contributions of other specific compound(s) associated with obstructive respiratory disease in these workers is still unresolved.
The strength of NIOSH is ability to respond to reports with combined occupational medicine, epidemiology, industrial hygiene [exposure characterization] and toxicology resources. The weakness is how long it takes.
The main point here is what should practitioners do to respond to clusters of occupational respiratory disease when they first emerge? The story parallels outbreaks of hypersensitivity pneumonitis in metal machining plants, lifeguard lung, legionaires disease, and even the post office anthrax experience.
Recently, victims at the index plant won judgements against International Flavors and Fragrances, for 10's of millions of dollars for devastating lung disease. Accounts of litigation can be found at http://www.butterflavoringlunginjury.com/
BrooklynDodger started this post noting the JOEH paper on characterization of exposure in the most recent issue, late 2005. The Dodger thought, how long has this been going on, and how long has the OH community been ignorant of the exposure levels? For interest, NIOSH reported
"Diacetyl, the predominant ketone in the plant, was present in
concentrations ranging from below detectable limits to 98 parts per million
parts air by volume (ppm), with a mean of 8.1 ppm (standard deviation 18.5 ppm).
The average ketone concentrations were highest in the microwave mixing room
where the 10 area samples had a mean diacetyl concentration of 37.8 ppm (SD 27.6
ppm)"
[The Dodger faults the authors for reporting, and the reviewers and editors for permitting them to report, arithmetic mean values rather than medians [easy to do], geometric means, or a mean value back calculated from the geometric mean and observed variance. The mean is less stable and suggests a higher exposure level over the population, thereby suggesting a lower unit risk.]
However, these data were reported in the NEJM paper in 2002.
An MMWR report appeared in April 2002, not much in advance of NEJM. The MMWR did report the geometric mean, which was reported as "The geometric mean air concentration of diacetyl was 18 parts per million parts air (ppm) in the room where the mixing tank was located, 1.3 ppm in the microwave-packaging area, and 0.02 ppm in other areas of the plant." [For epidemiologists, the Dodger notes that the geometric mean was 1/2 the arithmetic mean.]
http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5116a2.htm
Thus, the JOEH publication is an echo of previous information, either a product of "least publishable unit" publication or a slow editorial process at the journal.
[to be continued]
BrooklynDodger sympathizes with the team, especially the IH folks. Here's a devastating outbreak of disease. The most prominent chemical exposure is a food additive. Probably there's no toxicity data for this chemical, if there is it's probably feeding. [BrooklynDodger is going to work on this in the tox post]. It probably isn't that irritating and it does smell good. 100 ppm is a lot of organic vapor these days, but IH's think of 100 ppm as a TLV for a not specially toxic solvent.
>>>>>>>>>>>>>>>>>>>>>>
J Occup Environ Hyg. 2005 Mar;2(3):169-78.
Characterization of respiratory exposures at a microwave popcorn plant with cases of bronchiolitis obliterans.
Kullman G, Boylstein R, Jones W, Piacitelli C, Pendergrass S, Kreiss K.
National Institute for Occupational Safety and Health (NIOSH), Morgantown, West Virginia 26505, USA. gjk1@cdc.gov
Eight former workers from a microwave popcorn packaging plant were reported to have severe obstructive lung disease consistent with bronchiolitis obliterans. Investigations into respiratory exposures at this plant were done during August through November of 2000. ... Workers in the microwave production areas of the plant were exposed to particulates and a range of organic vapors from flavorings. The particles were comprised largely of salt and oil/grease particles. Respirable dust concentrations (area plus personal) in the microwave mixer job category, the highest job exposure category in the plant, ranged from 0.13 milligrams per cubic meter of air (mg/m3) to a high of 0.77 mg/m3. ...The predominant compounds identified in the microwave mixing room included the ketones diacetyl, methyl ethyl ketone, acetoin, and 2-nonanone, and acetic acid.
Diacetyl, the predominant ketone in the plant, was present in concentrations ranging from below detectable limits to 98 parts per million parts air by volume (ppm), with a mean of 8.1 ppm (standard deviation 18.5 ppm). The average ketone concentrations were highest in the microwave mixing room where the 10 area samples had a mean diacetyl concentration of 37.8 ppm (SD 27.6 ppm) and a mean acetoin concentration of 3.9 ppm (SD 4.3 ppm). These data show that workers involved in microwave popcorn packaging can be exposed to a complex mixture of VOCs from flavoring ingredients; animal studies show that diacetyl can cause airway epithelial injury, although the contributions of other specific compound(s) associated with obstructive respiratory disease in these workers is still unresolved.
Friday, October 28, 2005
Fine Particulate Carbon Black
Another ultrafine particle study from the labs in Rochester. These are 13 week studies among the rodent triumvers, rats, mice and hamsters.
BrooklynDodger questions whether particle count can be distiguished from particle area by studies of this type.
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Toxicol Sci. 2005 Sep 21; [Epub ahead of print]
Effects of Subchronically Inhaled Carbon Black in Three Species. I. Retention Kinetics, Lung Inflammation, and Histopathology.
Elder A, Gelein R, Finkelstein JN, Driscoll KE, Harkema J, Oberdorster G.
Department of Environmental Medicine, University of Rochester, Rochester, NY.
Exposure to high concentrations of carbon black (Cb) produces lung tumors in rats, but not mice or hamsters, presumably due to secondary genotoxic mechanisms involving persistent lung inflammation and injury.
... Particle retention kinetics, inflammation, and histopathology were examined in female rats, mice, and hamsters exposed for 13 weeks to high surface area Cb (HSCb) at doses chosen to span a no observable adverse effects level to particle overload (0, 1, 7, 50 mg/m(3), nominal concentrations). Rats were also exposed to low surface area Cb (50 mg/m(3), nominal; LSCb).
Retention and effects measurements were performed immediately after exposure and 3 and 11 months post-exposure; retention was also evaluated after 5 weeks of exposure. Significant decreases in body weight during exposure occurred only in hamsters exposed to high dose HSCb. Lung weights were increased in high dose Cb-exposed animals, but this persisted only in rats and mice up to the end of the study period. Equivalent or similar mass burdens were achieved in rats exposed to high dose HSCb and LSCb, whereas surface area burdens were equivalent for mid dose HSCb and LSCb. Prolonged retention was found in rats exposed to mid and high dose HSCb and to LSCb, but LSCb was cleared faster than HSCb. Retention was also prolonged in mice exposed to mid and high dose HSCb and in hamsters exposed to high dose HSCb. Lung inflammation and histopathology were more severe and prolonged in rats as compared to mice and hamsters and were similar in rats exposed to mid dose HSCb and LSCb. The results show that hamsters have the most efficient clearance mechanisms and least severe responses of the three species.
The results from rats also show that particle surface area is an important determinant of target tissue dose and, therefore, effects. From these results, a subchronic NOAEL of 1 mg/m(3) respirable HSCb (Printex 90) can be assigned to female rats, mice, and hamsters.
BrooklynDodger questions whether particle count can be distiguished from particle area by studies of this type.
>>>>>>>>>>>>>>>>>>>>>
Toxicol Sci. 2005 Sep 21; [Epub ahead of print]
Effects of Subchronically Inhaled Carbon Black in Three Species. I. Retention Kinetics, Lung Inflammation, and Histopathology.
Elder A, Gelein R, Finkelstein JN, Driscoll KE, Harkema J, Oberdorster G.
Department of Environmental Medicine, University of Rochester, Rochester, NY.
Exposure to high concentrations of carbon black (Cb) produces lung tumors in rats, but not mice or hamsters, presumably due to secondary genotoxic mechanisms involving persistent lung inflammation and injury.
... Particle retention kinetics, inflammation, and histopathology were examined in female rats, mice, and hamsters exposed for 13 weeks to high surface area Cb (HSCb) at doses chosen to span a no observable adverse effects level to particle overload (0, 1, 7, 50 mg/m(3), nominal concentrations). Rats were also exposed to low surface area Cb (50 mg/m(3), nominal; LSCb).
Retention and effects measurements were performed immediately after exposure and 3 and 11 months post-exposure; retention was also evaluated after 5 weeks of exposure. Significant decreases in body weight during exposure occurred only in hamsters exposed to high dose HSCb. Lung weights were increased in high dose Cb-exposed animals, but this persisted only in rats and mice up to the end of the study period. Equivalent or similar mass burdens were achieved in rats exposed to high dose HSCb and LSCb, whereas surface area burdens were equivalent for mid dose HSCb and LSCb. Prolonged retention was found in rats exposed to mid and high dose HSCb and to LSCb, but LSCb was cleared faster than HSCb. Retention was also prolonged in mice exposed to mid and high dose HSCb and in hamsters exposed to high dose HSCb. Lung inflammation and histopathology were more severe and prolonged in rats as compared to mice and hamsters and were similar in rats exposed to mid dose HSCb and LSCb. The results show that hamsters have the most efficient clearance mechanisms and least severe responses of the three species.
The results from rats also show that particle surface area is an important determinant of target tissue dose and, therefore, effects. From these results, a subchronic NOAEL of 1 mg/m(3) respirable HSCb (Printex 90) can be assigned to female rats, mice, and hamsters.
Thursday, October 27, 2005
Neurology Malpractice Claims
BrooklynDodger confesses not to have read this communication on malpractice claims for neurological causes in full text. Bottom line, investigators found more than half the claims were "authentic and preventable." Among the questions are whether there were a bunch of "maybes" in the pool.
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NEUROLOGY 2005;65:1284-1286
Neurologic patient safety: An in-depth study of malpractice claims
Thomas H. Glick, MD, Lee D. Cranberg, MD, Robert B. Hanscom, JD and Luke Sato, MD
From Harvard Medical School (Drs. Glick, Cranberg, and Sato), Boston, MA; and The Risk Management Foundation of the Harvard Medical Institutions, Inc. (Dr. Sato and R.B. Hanscom), Cambridge, MA.
Address correspondence and reprint requests to Dr. Thomas H. Glick, The Cambridge Hospital, 1493 Cambridge Street, Cambridge, MA 02139; e-mail: thomas_glick@hms.harvard.edu (image placeholder)
This in-depth study of neurologic malpractice claims indicated authentic, preventable patient harm in 24 of 42 cases, enabling comparison with larger but administratively abstracted summary reports. Principal findings included the common occurrence of outpatient events, lapses in communication with patients and other providers, the need for follow-through by the consultant neurologist even when not primarily responsible, the frequency of diagnostic errors, and pitfalls associated with imaging.
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NEUROLOGY 2005;65:1284-1286
Neurologic patient safety: An in-depth study of malpractice claims
Thomas H. Glick, MD, Lee D. Cranberg, MD, Robert B. Hanscom, JD and Luke Sato, MD
From Harvard Medical School (Drs. Glick, Cranberg, and Sato), Boston, MA; and The Risk Management Foundation of the Harvard Medical Institutions, Inc. (Dr. Sato and R.B. Hanscom), Cambridge, MA.
Address correspondence and reprint requests to Dr. Thomas H. Glick, The Cambridge Hospital, 1493 Cambridge Street, Cambridge, MA 02139; e-mail: thomas_glick@hms.harvard.edu (image placeholder)
This in-depth study of neurologic malpractice claims indicated authentic, preventable patient harm in 24 of 42 cases, enabling comparison with larger but administratively abstracted summary reports. Principal findings included the common occurrence of outpatient events, lapses in communication with patients and other providers, the need for follow-through by the consultant neurologist even when not primarily responsible, the frequency of diagnostic errors, and pitfalls associated with imaging.
Tuesday, October 25, 2005
Alcohol Associated with Retaining Marbles Among Elderly
BrooklynDodger calls to your attention another study showing the virtues of alcohol: In a representative elderly cohort over an average of 7 years, a pattern of mild-to-moderate drinking, compared to not drinking, was associated with lesser average decline in cognitive domains over the same period.”
Dodger has not gone to the full text to identify “moderate,” but whatever self reported is, they were probably pounding more. Additionally, there is no way out of the anti-hypothesis that people were drinking because they were healthier, rather than healthier because they were drinking.
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NEUROLOGY 2005;65:1210-1217Alcohol consumption and cognitive function in late life
A longitudinal community study
M. Ganguli, MD, MPH, J. Vander Bilt, MPH, J. A. Saxton, PhD, C. Shen, PhD and H. H. Dodge, PhD
From the Division of Geriatrics and Neuropsychiatry, Department of Psychiatry (Dr. Ganguli and J. Vander Bilt), Department of Neurology (Dr. Saxton), University of Pittsburgh School of Medicine, and Department of Epidemiology (Drs. Ganguli and Dodge), University of Pittsburgh Graduate School of Public Health, Pittsburgh, PA; and the Division of Biostatistics (Dr. Shen), School of Medicine, Indiana University, Indianapolis, IN.
Address correspondence and reprint requests to Dr. Mary Ganguli, Western Psychiatric Institute and Clinic, 3811 O’Hara Street, Pittsburgh, PA 15213-2593; e-mail: gangulim@upmc.edu (image placeholder)
Objective: To examine the association between alcohol use and cognitive decline in a longitudinal study of a representative elderly community sample free of dementia at baseline.
Methods: Cognitive functions and self-reported drinking habits were assessed at 2-year intervals over an average of 7 years of follow-up. Cognitive measures, grouped into composites, were examined in association with alcohol consumption. Trajectory analyses identified latent homogeneous groups with respect to alcohol use frequency over time, and their association with average decline over the same period in each cognitive domain. Models controlled for age, sex, education, depression, smoking, general mental status (Mini-Mental State Examination [MMSE]), performance on the given test at baseline, and subsequent new-onset dementia during follow-up.
Results: The authors found three homogeneous trajectories that they characterized as no drinking, minimal drinking, and moderate drinking. Few heavy drinkers were identified in this elderly cohort. Compared to no drinking, both minimal and moderate drinking were associated with lesser decline on the MMSE and Trailmaking tests. Minimal drinking was also associated with lesser decline on tests of learning and naming. These associations were more pronounced when comparing current drinkers to former drinkers (quitters) than to lifelong abstainers.
Conclusion: In a representative elderly cohort over an average of 7 years, a pattern of mild-to-moderate drinking, compared to not drinking, was associated with lesser average decline in cognitive domains over the same period.
Dodger has not gone to the full text to identify “moderate,” but whatever self reported is, they were probably pounding more. Additionally, there is no way out of the anti-hypothesis that people were drinking because they were healthier, rather than healthier because they were drinking.
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NEUROLOGY 2005;65:1210-1217Alcohol consumption and cognitive function in late life
A longitudinal community study
M. Ganguli, MD, MPH, J. Vander Bilt, MPH, J. A. Saxton, PhD, C. Shen, PhD and H. H. Dodge, PhD
From the Division of Geriatrics and Neuropsychiatry, Department of Psychiatry (Dr. Ganguli and J. Vander Bilt), Department of Neurology (Dr. Saxton), University of Pittsburgh School of Medicine, and Department of Epidemiology (Drs. Ganguli and Dodge), University of Pittsburgh Graduate School of Public Health, Pittsburgh, PA; and the Division of Biostatistics (Dr. Shen), School of Medicine, Indiana University, Indianapolis, IN.
Address correspondence and reprint requests to Dr. Mary Ganguli, Western Psychiatric Institute and Clinic, 3811 O’Hara Street, Pittsburgh, PA 15213-2593; e-mail: gangulim@upmc.edu (image placeholder)
Objective: To examine the association between alcohol use and cognitive decline in a longitudinal study of a representative elderly community sample free of dementia at baseline.
Methods: Cognitive functions and self-reported drinking habits were assessed at 2-year intervals over an average of 7 years of follow-up. Cognitive measures, grouped into composites, were examined in association with alcohol consumption. Trajectory analyses identified latent homogeneous groups with respect to alcohol use frequency over time, and their association with average decline over the same period in each cognitive domain. Models controlled for age, sex, education, depression, smoking, general mental status (Mini-Mental State Examination [MMSE]), performance on the given test at baseline, and subsequent new-onset dementia during follow-up.
Results: The authors found three homogeneous trajectories that they characterized as no drinking, minimal drinking, and moderate drinking. Few heavy drinkers were identified in this elderly cohort. Compared to no drinking, both minimal and moderate drinking were associated with lesser decline on the MMSE and Trailmaking tests. Minimal drinking was also associated with lesser decline on tests of learning and naming. These associations were more pronounced when comparing current drinkers to former drinkers (quitters) than to lifelong abstainers.
Conclusion: In a representative elderly cohort over an average of 7 years, a pattern of mild-to-moderate drinking, compared to not drinking, was associated with lesser average decline in cognitive domains over the same period.
Monday, October 24, 2005
Particles and Adverse Effects on Reproductive Health
Environmental Tobacco Smoke exposure compared to no ETS presents one of the few opportunities to measure human ultrafine and fine particle effects in the 50 ug/M3 range. Non-smoking, non ETS subjects are the lowest risk group, and so easiest to demonstrate an effect of whatever extra exposure. Otherwise, there's no strong reasons for piling on to tobacco and ETS.
Full text available on-line.
BrooklynDodger reminds readers that tobacco smoke is carcinogenic in bioassay only at extreme high levels of 200 milligrams/M3 in the rat, and not carcinogenic in the mouse and hamster. Among environmental particles, tobacco smoke is way less potent than competitors.
The importance of this report would be to identify an animal model to mimic this measured human effect, then use the animal model to evaluate a variety of particle exposures.
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Environ Health Perspect 113:412-417 (2005). doi:10.1289/ehp.7436 available via http://dx.doi.org/ [Online 14 January 2005]
Effect of Environmental Tobacco Smoke on Levels of Urinary Hormone Markers
Changzhong Chen,1 Xiaobin Wang,2 Lihua Wang,3 Fan Yang,4 Genfu Tang,4 Houxun Xing,4 Louise Ryan,5 Bill Lasley,6 James W. Overstreet,6 Joseph B. Stanford,7 and Xiping Xu1
1Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, USA; 2Department of Pediatrics, Northwestern University Feinberg School of Medicine and Children’s Memorial Hospital and Children’s Memorial Research Center, Chicago, Illinois, USA; 3Center for Ecogenetics and Reproductive Health, Beijing Medical University, Beijing, China; 4Institute for Biomedicine, Anhui Medical University, Anhui, China; 5Department of Biostatistics, Harvard School of Public Health, Boston, Massachusetts, USA; 6Institute of Toxicology and Environmental Health and Department of Obstetrics and Gynecology, School of Medicine, University of California, Davis, California, USA; 7Health Research Center, Department of Family and Preventive Medicine, University of Utah, Salt Lake City, Utah, USA
...Our recent study showed a dose-response relationship between environmental tobacco smoke (ETS) and the risk of early pregnancy loss. Smoking is known to affect female reproductive hormones. We explored whether ETS affects reproductive hormone profiles as characterized by urinary pregnanediol-3-glucuronide (PdG) and estrone conjugate (E1C) levels. We prospectively studied 371 healthy newly married nonsmoking women in China who intended to conceive and had stopped contraception. ... In nonconception cycles, cycles with ETS exposure had significantly lower urinary E1C levels ... compared with the cycles without ETS exposure. ... In conclusion, ETS exposure was associated with significantly lower urinary E1C levels among nonconception cycles, suggesting that the adverse reproductive effect of ETS may act partly through its antiestrogen effects. ...
Full text available on-line.
BrooklynDodger reminds readers that tobacco smoke is carcinogenic in bioassay only at extreme high levels of 200 milligrams/M3 in the rat, and not carcinogenic in the mouse and hamster. Among environmental particles, tobacco smoke is way less potent than competitors.
The importance of this report would be to identify an animal model to mimic this measured human effect, then use the animal model to evaluate a variety of particle exposures.
>>>>>>>>>>>>>>
Environ Health Perspect 113:412-417 (2005). doi:10.1289/ehp.7436 available via http://dx.doi.org/ [Online 14 January 2005]
Effect of Environmental Tobacco Smoke on Levels of Urinary Hormone Markers
Changzhong Chen,1 Xiaobin Wang,2 Lihua Wang,3 Fan Yang,4 Genfu Tang,4 Houxun Xing,4 Louise Ryan,5 Bill Lasley,6 James W. Overstreet,6 Joseph B. Stanford,7 and Xiping Xu1
1Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, USA; 2Department of Pediatrics, Northwestern University Feinberg School of Medicine and Children’s Memorial Hospital and Children’s Memorial Research Center, Chicago, Illinois, USA; 3Center for Ecogenetics and Reproductive Health, Beijing Medical University, Beijing, China; 4Institute for Biomedicine, Anhui Medical University, Anhui, China; 5Department of Biostatistics, Harvard School of Public Health, Boston, Massachusetts, USA; 6Institute of Toxicology and Environmental Health and Department of Obstetrics and Gynecology, School of Medicine, University of California, Davis, California, USA; 7Health Research Center, Department of Family and Preventive Medicine, University of Utah, Salt Lake City, Utah, USA
...Our recent study showed a dose-response relationship between environmental tobacco smoke (ETS) and the risk of early pregnancy loss. Smoking is known to affect female reproductive hormones. We explored whether ETS affects reproductive hormone profiles as characterized by urinary pregnanediol-3-glucuronide (PdG) and estrone conjugate (E1C) levels. We prospectively studied 371 healthy newly married nonsmoking women in China who intended to conceive and had stopped contraception. ... In nonconception cycles, cycles with ETS exposure had significantly lower urinary E1C levels ... compared with the cycles without ETS exposure. ... In conclusion, ETS exposure was associated with significantly lower urinary E1C levels among nonconception cycles, suggesting that the adverse reproductive effect of ETS may act partly through its antiestrogen effects. ...
Sunday, October 23, 2005
Hormesis - A New Model for Houdini Risk Assessment Developed by the Money Tox Industry
Hormesis is a new model "houdini risk assessment." Houdini risk assessements make a risk disappear, or permit a public health agency to escape from having to do anything difficult.
Hormesis assumes that low doses of toxic materials are therapeutic.
Well known are many therapeutic or health-promoting exposures - for example, Vitamin A or most pharmaceuticals - which are toxic at higher doses. Moderate alcohol consumption associates with much improved mortality experience compared to not drinking at all. Female-related estrogen contributes several extra years of lifespan at the cost of hugely increased risk of dying of breast, ovarian, uterine and cervical cancer.
From this does it follow that agents or exposures toxic at higher doses promote health at lower doses which don't present adverse effects? "Hormetics" argue yes.
This review, available in free full text, helps restore some balance of the money tox literature. Problem here is that compared to the massive carcinogenesis literature, the relevant literature here is nearly every dose response study in the pharamacology and toxicology world.
BrooklynDodger notes that below a no observed effect level, results have a 50/50 chance of reduced effect compared to the NOEL; two dose levels at 25% chance of both being "therapeutic" and 1/8 of a apparent j-shaped exposure-response.
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http://ehp.niehs.nih.gov/members/2005/7811/7811.pdf
Fundamental Flaws of Hormesis for Public Health Decisions
Kristina A. Thayer,1 Ronald Melnick,1 Kathy Burns,2 Devra Davis,3 and James Huff1
1National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services,Research Triangle Park, North Carolina, USA; 2Sciencecorps.org, Lexington, Massachusetts, USA; 3H. John Heinz III School of Public Policy & Management, Carnegie Mellon University, Pittsburgh, Pennsylvania, USA
Hormesis (defined operationally as low-dose stimulation, high-dose inhibition) is often used to
promote the notion that while high-level exposures to toxic chemicals could be detrimental to
human health, low-level exposures would be beneficial. Some proponents claim hormesis is an adaptive,
generalizable phenomenon and argue that the default assumption for risk assessments should be
that toxic chemicals induce stimulatory (i.e., “beneficial”) effects at low exposures. In many cases,
nonmonotonic dose–response curves are called hormetic responses even in the absence of any mechanistic
characterization of that response. Use of the term “hormesis,” with its associated descriptors,
distracts from the broader and more important questions regarding the frequency and interpretation
of nonmonotonic dose responses in biological systems. A better understanding of the biological basis
and consequences of nonmonotonic dose–response curves is warranted for evaluating human health
risks. The assumption that hormesis is generally adaptive is an oversimplification of complex biological
processes. Even if certain low-dose effects were sometimes considered beneficial, this should not
influence regulatory decisions to allow increased environmental exposures to toxic and carcinogenic
agents, given factors such as interindividual differences in susceptibility and multiplicity in exposures.
In this commentary we evaluate the hormesis hypothesis and potential adverse consequences
of incorporating low-dose beneficial effects into public health decisions. Key words: biphasic
dose response, hormesis, individual susceptibility, low-dose exposures, nonmonotonic dose response,
nonlinear dose response, public health, regulation, risk assessment. Environ Health Perspect
113:1271–1276 (2005). doi:10.1289/ehp.7811 available via http://dx.doi.org/ [Online 15 June 2005]
Hormesis assumes that low doses of toxic materials are therapeutic.
Well known are many therapeutic or health-promoting exposures - for example, Vitamin A or most pharmaceuticals - which are toxic at higher doses. Moderate alcohol consumption associates with much improved mortality experience compared to not drinking at all. Female-related estrogen contributes several extra years of lifespan at the cost of hugely increased risk of dying of breast, ovarian, uterine and cervical cancer.
From this does it follow that agents or exposures toxic at higher doses promote health at lower doses which don't present adverse effects? "Hormetics" argue yes.
This review, available in free full text, helps restore some balance of the money tox literature. Problem here is that compared to the massive carcinogenesis literature, the relevant literature here is nearly every dose response study in the pharamacology and toxicology world.
BrooklynDodger notes that below a no observed effect level, results have a 50/50 chance of reduced effect compared to the NOEL; two dose levels at 25% chance of both being "therapeutic" and 1/8 of a apparent j-shaped exposure-response.
>>>>>>>>>>>>>>>>>>>>>>>>>
http://ehp.niehs.nih.gov/members/2005/7811/7811.pdf
Fundamental Flaws of Hormesis for Public Health Decisions
Kristina A. Thayer,1 Ronald Melnick,1 Kathy Burns,2 Devra Davis,3 and James Huff1
1National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services,Research Triangle Park, North Carolina, USA; 2Sciencecorps.org, Lexington, Massachusetts, USA; 3H. John Heinz III School of Public Policy & Management, Carnegie Mellon University, Pittsburgh, Pennsylvania, USA
Hormesis (defined operationally as low-dose stimulation, high-dose inhibition) is often used to
promote the notion that while high-level exposures to toxic chemicals could be detrimental to
human health, low-level exposures would be beneficial. Some proponents claim hormesis is an adaptive,
generalizable phenomenon and argue that the default assumption for risk assessments should be
that toxic chemicals induce stimulatory (i.e., “beneficial”) effects at low exposures. In many cases,
nonmonotonic dose–response curves are called hormetic responses even in the absence of any mechanistic
characterization of that response. Use of the term “hormesis,” with its associated descriptors,
distracts from the broader and more important questions regarding the frequency and interpretation
of nonmonotonic dose responses in biological systems. A better understanding of the biological basis
and consequences of nonmonotonic dose–response curves is warranted for evaluating human health
risks. The assumption that hormesis is generally adaptive is an oversimplification of complex biological
processes. Even if certain low-dose effects were sometimes considered beneficial, this should not
influence regulatory decisions to allow increased environmental exposures to toxic and carcinogenic
agents, given factors such as interindividual differences in susceptibility and multiplicity in exposures.
In this commentary we evaluate the hormesis hypothesis and potential adverse consequences
of incorporating low-dose beneficial effects into public health decisions. Key words: biphasic
dose response, hormesis, individual susceptibility, low-dose exposures, nonmonotonic dose response,
nonlinear dose response, public health, regulation, risk assessment. Environ Health Perspect
113:1271–1276 (2005). doi:10.1289/ehp.7811 available via http://dx.doi.org/ [Online 15 June 2005]
Saturday, October 22, 2005
Biomass Related Effects - Wet Building Syndrome
BrooklynDodger notes this paper is available to all free in full text. This account should be read with Katrina remediation and biomass remediation generally in mind.
The authors do us a service by putting some actual rates as well as relative rates in the abstract.
There's no mention of environmental measurements or conditions. Typically total mold is higher outside than inside, or in a molded or water intruded building. Also typically, the mold organisms inside the intruded space are different from those outside. There's lots of different mold organisms inside and outside, they are identified to species level. "Species" is a shaky concept for non-sexually reproducing organisms.
[Regarding outdoor vs. indoor mold, readers are reminded that huge numbers of people suffer from the outdoor mold, many taking performance-impairing anti-histamines in large doses in order to function at work and in normal life.]
BrooklynDodger frames the issue of mold or water intrusion this way. There's no [practical]population threshold for respiratory reaction to a biological contaminant, or for infection - the exposure-response relationship goes to very low levels. A single microorganism has a non-zero probability of starting an infection. Subpopulations are hypersensitive or become hypersensitive to sensitizing materials. This sensitivity may be through an allergic type mechanism or some other unknown mechanism. Perhaps there are unknown and therefore unmeasurable vapor phase contaminants.
The large number of agents, large number of [hypothetical] sensitive sub populations, and multiplicative combinations blunt ability to determine exposure response at the individual wet building level. Most of the agents aren't measured because they are not known, and can only be detected by the reactions of the sensitive people.
Likely these unidentified agents, under these conditions, can't be removed to the degree that all sensitives will be symptom free, although the sensitives may tolerate the environment if their livelihood depends on it. [It's circular, they are sensitives because they react, not from any external observable feature.]
>>>>>>>>>>>>>>>>>>>>
Benchmarks:
The comparison population was the National Health and Nutrition Epidemiologic Survey, NHANES. Prevalence of various answers in this population ranged from current ashma, 13% [2.4 times NHANES predicted], ever asthma 18% [2.2 times], up to "Wheezing, nose, or eye symptoms better on days off work" 72.1% [3.4 times.]
Thus the basic OM question "Is this problem better or worse at any particular time" - strongest answer being "best while on extended time away from workplace, worst the day after returning from extended time away..." is vindicated at the strongest predictor.
>>>>>>>>>>>>>>>>>
On another front, these investigators appear to have used the job content questionnaire. This is very suspect, although more applicable to an office population than an industrial population.
>>>>>>>>>>>>>>>>>>>>
Environ Health Perspect. 2005 Apr;113(4):485-90.
Respiratory morbidity in office workers in a water-damaged building.
Cox-Ganser JM, White SK, Jones R, Hilsbos K, Storey E, Enright PL, Rao CY, Kreiss K.
Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, Morgantown, West Virginia 26505, USA. jjc8@cdc.gov
We conducted a study on building-related respiratory disease and associated social impact in an office building with water incursions in the northeastern United States. ...Compared with the U.S. adult population, prevalence ratios were 2.2-2.5 for wheezing, lifetime asthma, and current asthma, 3.3 for adult-onset asthma, and 3.4 for symptoms improving away from work (p <> Occupancy of the water-damaged building was associated with onset and exacerbation of respiratory conditions, confirmed by objective medical tests. The morbidity and lost work time burdened both employees and employers.
The authors do us a service by putting some actual rates as well as relative rates in the abstract.
There's no mention of environmental measurements or conditions. Typically total mold is higher outside than inside, or in a molded or water intruded building. Also typically, the mold organisms inside the intruded space are different from those outside. There's lots of different mold organisms inside and outside, they are identified to species level. "Species" is a shaky concept for non-sexually reproducing organisms.
[Regarding outdoor vs. indoor mold, readers are reminded that huge numbers of people suffer from the outdoor mold, many taking performance-impairing anti-histamines in large doses in order to function at work and in normal life.]
BrooklynDodger frames the issue of mold or water intrusion this way. There's no [practical]population threshold for respiratory reaction to a biological contaminant, or for infection - the exposure-response relationship goes to very low levels. A single microorganism has a non-zero probability of starting an infection. Subpopulations are hypersensitive or become hypersensitive to sensitizing materials. This sensitivity may be through an allergic type mechanism or some other unknown mechanism. Perhaps there are unknown and therefore unmeasurable vapor phase contaminants.
The large number of agents, large number of [hypothetical] sensitive sub populations, and multiplicative combinations blunt ability to determine exposure response at the individual wet building level. Most of the agents aren't measured because they are not known, and can only be detected by the reactions of the sensitive people.
Likely these unidentified agents, under these conditions, can't be removed to the degree that all sensitives will be symptom free, although the sensitives may tolerate the environment if their livelihood depends on it. [It's circular, they are sensitives because they react, not from any external observable feature.]
>>>>>>>>>>>>>>>>>>>>
Benchmarks:
The comparison population was the National Health and Nutrition Epidemiologic Survey, NHANES. Prevalence of various answers in this population ranged from current ashma, 13% [2.4 times NHANES predicted], ever asthma 18% [2.2 times], up to "Wheezing, nose, or eye symptoms better on days off work" 72.1% [3.4 times.]
Thus the basic OM question "Is this problem better or worse at any particular time" - strongest answer being "best while on extended time away from workplace, worst the day after returning from extended time away..." is vindicated at the strongest predictor.
>>>>>>>>>>>>>>>>>
On another front, these investigators appear to have used the job content questionnaire. This is very suspect, although more applicable to an office population than an industrial population.
>>>>>>>>>>>>>>>>>>>>
Environ Health Perspect. 2005 Apr;113(4):485-90.
Respiratory morbidity in office workers in a water-damaged building.
Cox-Ganser JM, White SK, Jones R, Hilsbos K, Storey E, Enright PL, Rao CY, Kreiss K.
Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, Morgantown, West Virginia 26505, USA. jjc8@cdc.gov
We conducted a study on building-related respiratory disease and associated social impact in an office building with water incursions in the northeastern United States. ...Compared with the U.S. adult population, prevalence ratios were 2.2-2.5 for wheezing, lifetime asthma, and current asthma, 3.3 for adult-onset asthma, and 3.4 for symptoms improving away from work (p <> Occupancy of the water-damaged building was associated with onset and exacerbation of respiratory conditions, confirmed by objective medical tests. The morbidity and lost work time burdened both employees and employers.
Saturday, October 15, 2005
Bird Flu
We are maybe moving in the direction of syndromic surveillance. Multiple incidents of workplace caused respiratory disease have been dismissed as the "flu." The flu that's here kills about 35,000 a year, chump casualties compared to the millions from possible pandemic bird flu, but serious enough.
Until the media is educated on respirators that work, how can we expect the public to be? These, taken from MSNBC, seem to have a nose clip, but only one strap so they can't work.
That is one really scary looking sick or dead bird. Wonder what country?
Thursday, October 13, 2005
For employed people, 38% of injuries occur at work
The National Safety Council, and others, have been pushing for diversion of occupational safety and health resources to off-the-job injury prevention programs. BrooklynDodger concurs in part and dissents in part.
Dissent is, resources for occupational health and safety are meager, and people who work safety and health occupy organizational niches which won’t be filled if they look on something else. Second is, off the job initiatives launched on the job are virtually all low level of control, blame the victim exhortations.
Off the job injury deserves more emphasis in public health circles. Problem is the higher level initiatives are even more politically contentious than OSHA. To control fatal injuries, you are talking about controlling guns and cars.
>>>>>>>>>>>>>>>>>>>>>
Am J Public Health. 2005 Jul;95(7):1213-9.
Injuries at work in the US adult population: contributions to the total injury burden.Smith GS, Wellman HM, Sorock GS, Warner M, Courtney TK, Pransky GS, Fingerhut LA.Liberty Mutual Research Institute for Safety, Hopkinton, MA 01748, USA. gordon. smith@libertymutual.comWe used the 1997-1999 National Health Interview Survey (NHIS) to estimate injury rates and proportions of work-related vs non-work-related injuries. An estimated 19.4 million medically treated injuries occurred annually to working-age adults (11.7 episodes per 100 persons; 29%, or 5.5 million 4.5 per 100 persons, occurred at work and varied by gender, age, and race/ethnicity. Among employed persons, 38% of injuries occurred at work, and among employed men aged 55-64 years, 49% of injuries occurred at work. Study estimates of days away from work after injury were 1.8 times higher than the Bureau of Labor Statistics (BLS) workplace-based estimates and 1.4 times as high as BLS estimates for private industry.
Dissent is, resources for occupational health and safety are meager, and people who work safety and health occupy organizational niches which won’t be filled if they look on something else. Second is, off the job initiatives launched on the job are virtually all low level of control, blame the victim exhortations.
Off the job injury deserves more emphasis in public health circles. Problem is the higher level initiatives are even more politically contentious than OSHA. To control fatal injuries, you are talking about controlling guns and cars.
>>>>>>>>>>>>>>>>>>>>>
Am J Public Health. 2005 Jul;95(7):1213-9.
Injuries at work in the US adult population: contributions to the total injury burden.Smith GS, Wellman HM, Sorock GS, Warner M, Courtney TK, Pransky GS, Fingerhut LA.Liberty Mutual Research Institute for Safety, Hopkinton, MA 01748, USA. gordon. smith@libertymutual.comWe used the 1997-1999 National Health Interview Survey (NHIS) to estimate injury rates and proportions of work-related vs non-work-related injuries. An estimated 19.4 million medically treated injuries occurred annually to working-age adults (11.7 episodes per 100 persons; 29%, or 5.5 million 4.5 per 100 persons, occurred at work and varied by gender, age, and race/ethnicity. Among employed persons, 38% of injuries occurred at work, and among employed men aged 55-64 years, 49% of injuries occurred at work. Study estimates of days away from work after injury were 1.8 times higher than the Bureau of Labor Statistics (BLS) workplace-based estimates and 1.4 times as high as BLS estimates for private industry.
Wednesday, October 12, 2005
Asbestosis and silicosis in Foundry Workers
Asbestosis and silicosis among foundry workers
Can silicosis and asbestosis be seen in the same chest x-ray? This rises from the controversy on silica lawsuits being used to trash plaintiff’s lawyers in the NY Times. It’s also a question in the arcane art of B reading. It’s also a question of whether other dust might cause asbestosis like changes, or whether there is an occult source of asbestos [or some other fiber] in foundry sand.
This study consisted of reading the chest x-rays of 1,072 current and retired workers at a foundry. Sixty, or 6% had dust disease on chest x-ray; 12% of those with more than 30 years service had dust disease. Of these, 28 were thought to have silica related changes, 8 had asbestosis and 24 had pleural plaques. The asbestos changes were found with greater frequency by those in maintenance jobs, but some were found in production workers without known exposure to asbestos.
Comment: Silica and asbestos x-ray changes occur in the same population. It’s likely individual x-rays presented a mixed picture. Asbestos-related changes were not expected with this prevalence based on known exposures.
------------------------------------------------------------
Am J Epidemiol. 1996 Nov 1;144(9):890-900.
Related Articles,(image placeholder)Links
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.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.
f:\dept\h&s\home\fmirer\docs\doc\asbestosis and silicosis among foundry workers.doc
Can silicosis and asbestosis be seen in the same chest x-ray? This rises from the controversy on silica lawsuits being used to trash plaintiff’s lawyers in the NY Times. It’s also a question in the arcane art of B reading. It’s also a question of whether other dust might cause asbestosis like changes, or whether there is an occult source of asbestos [or some other fiber] in foundry sand.
This study consisted of reading the chest x-rays of 1,072 current and retired workers at a foundry. Sixty, or 6% had dust disease on chest x-ray; 12% of those with more than 30 years service had dust disease. Of these, 28 were thought to have silica related changes, 8 had asbestosis and 24 had pleural plaques. The asbestos changes were found with greater frequency by those in maintenance jobs, but some were found in production workers without known exposure to asbestos.
Comment: Silica and asbestos x-ray changes occur in the same population. It’s likely individual x-rays presented a mixed picture. Asbestos-related changes were not expected with this prevalence based on known exposures.
------------------------------------------------------------
Am J Epidemiol. 1996 Nov 1;144(9):890-900.
Related Articles,(image placeholder)Links
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.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.
f:\dept\h&s\home\fmirer\docs\doc\asbestosis and silicosis among foundry workers.doc
Monday, October 10, 2005
Increased Colorectal Cancer Observed Among Asbestos Exposed Workers
BrooklynDodger couldn’t retrieve the full text for this.
Does asbestos exposure cause colorectal cancer? This remains in dispute. The CARET study – a failed attempt to demonstrate chemoprevention of lung cancer by Vitamin A – provides information. Bottom line, asbestos exposed workers suffered increased colorectal cancer. The findings are limited to heavy smokers because only heavy smokers were permitted in the study.
>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
Am J Epidemiol. 2005 Sep 21; [Epub ahead of print]
Evidence for Excess Colorectal Cancer Incidence among Asbestos-exposed Men in the Beta-Carotene and Retinol Efficacy Trial.
Aliyu OA, Cullen MR, Barnett MJ, Balmes JR, Cartmel B, Redlich CA, Brodkin CA, Barnhart S, Rosenstock L, Israel L, Goodman GE, Thornquist MD, Omenn GS.Yale Occupational and Environmental Medicine Program and the Cancer Center, Yale University School of Medicine, New Haven, CT.The relation between asbestos exposure and colorectal cancer remains controversial. The authors of this 1984-2004 US study examined the association among 3,897 occupationally exposed participants in the Beta-Carotene and Retinol Efficacy Trial (CARET) for chemoprevention of lung cancer, followed prospectively for 10-18 years. When a Cox stratified proportional hazards model was used, risks of colorectal cancer were elevated among male heavy smokers exposed to asbestos. Their relative risk was 1.36 (95% confidence interval: 0.96, 1.93) when compared with that for CARET heavy smokers not exposed to asbestos, after adjusting for age, smoking history, and intervention arm. The presence of asbestos-induced pleural plaques at baseline was associated with a relative risk of 1.54 (95% confidence interval: 0.99, 2.40); colorectal cancer risk also increased with worsening pulmonary asbestosis (p = 0.03 for trend). A dose-response trend based on years of asbestos exposure was less evident. Nonetheless, these data suggest that colorectal cancer risk is elevated among men occupationally exposed to asbestos, especially those with evidence of nonmalignant asbestos-associated radiographic changes.
Sunday, October 09, 2005
New York Times and Diagnosis of Silicosis and Asbestosis
BrooklynDodger posts this to a science blog because the silicosis-asbestosis litigation debate turns on science and diagnostic criteria.
Jonathan Glater has gotten major inches attacking the plaintiff’s bar and plaintiff's medical experts over silica litigation. In the article below, he at least left out his canonical attack on how long was spent reading x-rays ["a few minutes' - which is what a B-reader does], and on doctors making judgements based on "reading only reports" [which is what an internist should do with a radiologist report, or pathology.]
>>>>>>>>>>>>>>>>>>>>>>>>
http://www.nytimes.com/packages/pdf/business/MDL-1553.pdf
The Tort Wars, at a Turning Point
by JONATHAN D. GLATER
Published: October 9, 2005
FOR the lawyers who file lawsuits against corporations, it looked like the next big thing - the next fen-phen, asbestos or even tobacco, the mother of all jackpots.
Like the lawsuits involving asbestos, the fire-retardant material that when inhaled can cause a horrible lung cancer, the new suits involved a substance that under certain circumstances could harm the lungs: silica, a purified sand used as a cleaning abrasive as well as in making glass, paint, ceramics and other materials. Silica dust, when inhaled, can lodge in the lungs, causing silicosis, a disabling and often fatal lung disease.
For the companies facing litigation, it looked like a repeat nightmare. After all, settling asbestos claims - more than 700,000 have been filed over the last 30 years - has cost more than $70 billion, according to the RAND Corporation. Of that amount, RAND estimates that nearly one-third has gone to plaintiffs' lawyers.
…
Judge Jack not only called for sanctions on one of the plaintiffs'-side law firms, but she also slammed the whole process that led to the claims landing in court in the first place. The medical findings underlying the claims, based on X-ray screenings paid for by lawyers looking for potential clients, were worthless, she wrote.
…
Mr. Krutz and Mr. Mulholland asked Judge Jack if they could question one of the doctors, George H. Martindale, of Mobile, Ala. Dr. Martindale had diagnosed more than 3,600 people with silicosis, according to court documents, and Mr. Mulholland had found that some of them had previously submitted asbestos claims.
The deposition, on Oct. 29, 2004, went better than the defense lawyers could have hoped. At one point, Mr. Mulholland asked: "Would it be fair to say that this appears to state a clinical diagnosis of silicosis when, in fact, that's not what you did?" Dr. Martindale answered: "Correct."
Under the questioning, Dr. Martindale said he never talked to any of the claimants whose X-rays he read, either to learn their work histories or to notify them if he determined that they suffered from silicosis. Pushing further, Mr. Mulholland asked Dr. Martindale whether he stood by the diagnoses. Dr. Martindale responded, "If another physician hadn't established a diagnosis of silicosis/asbestosis, I would withdraw that. I would - I would say that I am personally not making a diagnosis of asbestosis or silicosis."
…
Several doctors on the witness stand withdrew their diagnoses and said they had never interviewed the people whose X-rays, or in some cases just reports on their X-rays, they had analyzed. In some cases, doctors could not explain how they diagnosed asbestosis in a claimant at one time and silicosis at a later date, even when looking at the same X-ray.
…
It was a rare courtroom moment, one usually reserved for novels or movies. Mr. Mulholland recalled that when he asked one doctor about two differing diagnoses based on the same X-ray, the doctor, Ray A. Harron, explained the discrepancy by saying he made the diagnoses on "widely separated dates."
When Dr. Harron was asked about another case of a person who first received a diagnosis of one disease, and then of the other, Judge Jack interrupted the questioning to ask what happened to the first illness. "Well," she said, "where did it go?"
Dr. Harron responded, "Like I say, I don't know." Shortly after that, Dr. Harron cut his testimony short, citing the need to retain his own lawyer. He did not return calls seeking comment on the silica proceedings. In a deposition last year, Dr. Harron said he charged up to $125 for each case he reviewed; the amount was not affected by his diagnosis. If he had to travel to make a diagnosis, he said he might set a minimum fee to cover his travel costs and his time.
Diagnoses from Dr. Harron and one other doctor accounted for about 90 percent of the silica diagnoses, and they had previously diagnosed thousands of people - some of them the same people - with asbestosis.
Jonathan Glater has gotten major inches attacking the plaintiff’s bar and plaintiff's medical experts over silica litigation. In the article below, he at least left out his canonical attack on how long was spent reading x-rays ["a few minutes' - which is what a B-reader does], and on doctors making judgements based on "reading only reports" [which is what an internist should do with a radiologist report, or pathology.]
BrooklynDodger checked the NIOSH registry of B-readers for Drs Martindale and Harron attacked below. There is no Martindale at all in the registry, and no Ray Harron.
BrooklynDodger has no doubt that large scale screening of silica exposed workers would find substantial fractions of bad chest x rays among those with 20 year latency from first exposure. While the Times notes a decline in "silicosis" deaths, most of the xs respiratory mortality among foundry workers and likely others, comes from other diagnoses. Most is likely silica related.
Although B readers are adamant about distinguishing asbestos patterns from silica patterns, the Dodger wonders, and also wonders about a mixed picture.
The Dodger concedes there's something cheesy about these wholesale medical reports. Or diagnosing without interview on symptoms or history of exposure. It's like one cop signing the arrest reports of hundreds of people arrested at a demonstration, so only one has to show up in court.
The opinion is downloadable below.
>>>>>>>>>>>>>>>>>>>>>>>>
http://www.nytimes.com/packages/pdf/business/MDL-1553.pdf
The Tort Wars, at a Turning Point
by JONATHAN D. GLATER
Published: October 9, 2005
FOR the lawyers who file lawsuits against corporations, it looked like the next big thing - the next fen-phen, asbestos or even tobacco, the mother of all jackpots.
Like the lawsuits involving asbestos, the fire-retardant material that when inhaled can cause a horrible lung cancer, the new suits involved a substance that under certain circumstances could harm the lungs: silica, a purified sand used as a cleaning abrasive as well as in making glass, paint, ceramics and other materials. Silica dust, when inhaled, can lodge in the lungs, causing silicosis, a disabling and often fatal lung disease.
For the companies facing litigation, it looked like a repeat nightmare. After all, settling asbestos claims - more than 700,000 have been filed over the last 30 years - has cost more than $70 billion, according to the RAND Corporation. Of that amount, RAND estimates that nearly one-third has gone to plaintiffs' lawyers.
…
Judge Jack not only called for sanctions on one of the plaintiffs'-side law firms, but she also slammed the whole process that led to the claims landing in court in the first place. The medical findings underlying the claims, based on X-ray screenings paid for by lawyers looking for potential clients, were worthless, she wrote.
…
Mr. Krutz and Mr. Mulholland asked Judge Jack if they could question one of the doctors, George H. Martindale, of Mobile, Ala. Dr. Martindale had diagnosed more than 3,600 people with silicosis, according to court documents, and Mr. Mulholland had found that some of them had previously submitted asbestos claims.
The deposition, on Oct. 29, 2004, went better than the defense lawyers could have hoped. At one point, Mr. Mulholland asked: "Would it be fair to say that this appears to state a clinical diagnosis of silicosis when, in fact, that's not what you did?" Dr. Martindale answered: "Correct."
Under the questioning, Dr. Martindale said he never talked to any of the claimants whose X-rays he read, either to learn their work histories or to notify them if he determined that they suffered from silicosis. Pushing further, Mr. Mulholland asked Dr. Martindale whether he stood by the diagnoses. Dr. Martindale responded, "If another physician hadn't established a diagnosis of silicosis/asbestosis, I would withdraw that. I would - I would say that I am personally not making a diagnosis of asbestosis or silicosis."
…
Several doctors on the witness stand withdrew their diagnoses and said they had never interviewed the people whose X-rays, or in some cases just reports on their X-rays, they had analyzed. In some cases, doctors could not explain how they diagnosed asbestosis in a claimant at one time and silicosis at a later date, even when looking at the same X-ray.
…
It was a rare courtroom moment, one usually reserved for novels or movies. Mr. Mulholland recalled that when he asked one doctor about two differing diagnoses based on the same X-ray, the doctor, Ray A. Harron, explained the discrepancy by saying he made the diagnoses on "widely separated dates."
When Dr. Harron was asked about another case of a person who first received a diagnosis of one disease, and then of the other, Judge Jack interrupted the questioning to ask what happened to the first illness. "Well," she said, "where did it go?"
Dr. Harron responded, "Like I say, I don't know." Shortly after that, Dr. Harron cut his testimony short, citing the need to retain his own lawyer. He did not return calls seeking comment on the silica proceedings. In a deposition last year, Dr. Harron said he charged up to $125 for each case he reviewed; the amount was not affected by his diagnosis. If he had to travel to make a diagnosis, he said he might set a minimum fee to cover his travel costs and his time.
Diagnoses from Dr. Harron and one other doctor accounted for about 90 percent of the silica diagnoses, and they had previously diagnosed thousands of people - some of them the same people - with asbestosis.
TV and Naps: Science of Parenting
BrooklynDodger found another journal which might be worth following for public health information. Pediatrics as a specialty seems to either attract or impose more of a public health orientation than others.
How much TV to let the child watch is among the serious day to day questions in parenting. The paper abstracted below applies science to this.
The Dodger confesses not to know the methods of the National Survey of Early Childhood health; Dodger suspects it’s interview data with parents. Here we find that bout 1/3 of parents report irregular naptime or bedtime schedules. There’s no data included on duration of naps or sleep. On average, they report children less than 1 year old “watching” television about 1 hour per day, up to 2 ½ hours a day for those 2-3 years old. Those of us with kids need to think back to those days to characterize the environment and purpose of exposure to TV; for the older kids it’s likely a combination of immobilization and baby sitting.
Assuming these odds ratios are per hour, there’s about a 30% increase in risk of irregular bedtime for 3 hours of TV. The Dodger can’t find the risk at 0 hours of TV in the paper.
Much the strongest risk factor for irregular sleeping times was irregular meal times, present in 25% of the population generating a risk ratio of 2.5. Education beyond high school (80% of the population) generated a risk ratio of 0.6
Pairwise comparisons would have been interested. Cross tabs between irregular mealtime and TV would illuminate the interpretation.
All in all, there’s little reason to think that the parental value of relief with the kid in front of the TV outweighs the parental detriment of irregular naps and bedtime.
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Pediatrics 2005; 116: 851-856
The Association Between Television Viewing and Irregular Sleep Schedules Among Children Less Than 3 Years of Age
Darcy A. Thompson, MD, MPH*,and Dimitri A. Christakis, MD, MPH
* Robert Wood Johnson Clinical Scholars Program
Department of Pediatric Child Health Institute, University of Washington, Seattle, Washington|Children’s Hospital and Regional Medical Center, Seattle, Washington
…We used data from the National Survey of Early Childhood Health, a nationally representative, cross-sectional study of the health and health care of children 4 to 35 months of age. Our main outcome measures were whether children had irregular naptime and be…Data were available for 2068 children. Thirty-four percent of all children had irregular naptime schedules, and 27% had irregular bedtime schedules. Mean hours of television viewing per day were as follows: 0.9 hours/day … for children <12 months of age, 1.6 hours/day …for children 12 to 23 months of age, and 2.3 hours/day … for children 24 to 35 months of age. In our logistic regression model, the number of hours of television watched per day was associated with both an irregular naptime schedule (odds ratio: 1.09; 95% CI: 1.01–1.18) and an irregular bedtime schedule (odds ratio: 1.13; 95% CI: 1.04–1.24).
Conclusions. Television viewing among infants and toddlers is associated with irregular sleep schedules. More research is warranted to determine whether this association is causal.
How much TV to let the child watch is among the serious day to day questions in parenting. The paper abstracted below applies science to this.
The Dodger confesses not to know the methods of the National Survey of Early Childhood health; Dodger suspects it’s interview data with parents. Here we find that bout 1/3 of parents report irregular naptime or bedtime schedules. There’s no data included on duration of naps or sleep. On average, they report children less than 1 year old “watching” television about 1 hour per day, up to 2 ½ hours a day for those 2-3 years old. Those of us with kids need to think back to those days to characterize the environment and purpose of exposure to TV; for the older kids it’s likely a combination of immobilization and baby sitting.
Assuming these odds ratios are per hour, there’s about a 30% increase in risk of irregular bedtime for 3 hours of TV. The Dodger can’t find the risk at 0 hours of TV in the paper.
Much the strongest risk factor for irregular sleeping times was irregular meal times, present in 25% of the population generating a risk ratio of 2.5. Education beyond high school (80% of the population) generated a risk ratio of 0.6
Pairwise comparisons would have been interested. Cross tabs between irregular mealtime and TV would illuminate the interpretation.
All in all, there’s little reason to think that the parental value of relief with the kid in front of the TV outweighs the parental detriment of irregular naps and bedtime.
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Pediatrics 2005; 116: 851-856
The Association Between Television Viewing and Irregular Sleep Schedules Among Children Less Than 3 Years of Age
Darcy A. Thompson, MD, MPH*,and Dimitri A. Christakis, MD, MPH
* Robert Wood Johnson Clinical Scholars Program
Department of Pediatric Child Health Institute, University of Washington, Seattle, Washington|Children’s Hospital and Regional Medical Center, Seattle, Washington
…We used data from the National Survey of Early Childhood Health, a nationally representative, cross-sectional study of the health and health care of children 4 to 35 months of age. Our main outcome measures were whether children had irregular naptime and be…Data were available for 2068 children. Thirty-four percent of all children had irregular naptime schedules, and 27% had irregular bedtime schedules. Mean hours of television viewing per day were as follows: 0.9 hours/day … for children <12 months of age, 1.6 hours/day …for children 12 to 23 months of age, and 2.3 hours/day … for children 24 to 35 months of age. In our logistic regression model, the number of hours of television watched per day was associated with both an irregular naptime schedule (odds ratio: 1.09; 95% CI: 1.01–1.18) and an irregular bedtime schedule (odds ratio: 1.13; 95% CI: 1.04–1.24).
Conclusions. Television viewing among infants and toddlers is associated with irregular sleep schedules. More research is warranted to determine whether this association is causal.
Saturday, October 08, 2005
Media Violence
Those who scapegoat the media for crime focus on the programs. This study focused on the commercials, with an elaborate sampling scheme to pick the commercials children might watch during sports events [which themselves often contain violent behavior.] The raters found that 14% of commercials displayed unsafe behavior and 6% portrayed violence. Of course, you’re never able to view just one commercial. Using commercial breaks as a unit, 49% contained at least one bad actor. The super bowl had 4 times as many unsafe or violent commercials as the Masters Golf Tournament [which is a snoozer to begin with.] Commercials for cars were amongst the worst for products.
Content media is still a culprit. Only 18% of reviewed commercials advertised movies or television programs, yet these commercials accounted for 86% of all violent commercials. Forty-eight percent of commercials that contained violence were for movies, and an additional 38% were for television programs. Of course, if you want guys to watch movies, what kind of movies are you going to advertise.
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Pediatrics. 2004 Dec;114(6):e694-8.
Unsafe and violent behavior in commercials aired during televised major sporting events.Tamburro RF, Gordon PL, D'Apolito JP, Howard SC.Division of Critical Care Medicine, St Jude Children's Research Hospital, and Le Bonheur Children's Medical Center, 332 North Lauderdale, Memphis, Tennessee 38105-2784, USA. robert.tamburro@stjude.org… For sporting events with >3 programs in the top 50 (NFL regular season games, NFL playoff games, Winter Olympic events, and Major League Baseball World Series)…commercials … were reviewed at standard speed for unsafe behavior or violence. …Commercials were categorized according to the product being advertised. Unsafe behavior was simply defined as any action that could have harmful consequences or that contravened the injury prevention recommendations of national organizations. ... The proportion of commercials that depicted unsafe behavior and/or violence during each sporting event was compared with the proportion of such commercials that were observed during the Masters Golf Tournament (which had the lowest proportion of commercials depicting such behavior). The proportion of commercials that contained violent/unsafe behavior for each advertised product was compared with the proportion of such commercials that advertised food or nonalcoholic beverages…. Of the 1185 commercials assessed, 14% (n = 165) displayed unsafe behavior and 6% (n = 66) depicted violence. Of the 322 commercial breaks, 158 (49%) contained at least 1 commercial showing unsafe behavior or violence. … The Super Bowl had the highest proportion of such commercials, and the Masters Golf Tournament had the least (relative risk: 4.3; 95% confidence interval: 1.4-12.5). The Masters Golf Tournament was noteworthy for the complete absence of violent commercials. Only 18% of reviewed commercials advertised movies or television programs, yet these commercials accounted for 86% of all violent commercials. Forty-eight percent of commercials that contained violence were for movies, and an additional 38% were for television programs. … Several categories of commercials portrayed unsafe behaviors; commercials for automobiles accounted for the most. In 8 different categories, 10% or more of the commercials depicted unsafe behavior, …
Content media is still a culprit. Only 18% of reviewed commercials advertised movies or television programs, yet these commercials accounted for 86% of all violent commercials. Forty-eight percent of commercials that contained violence were for movies, and an additional 38% were for television programs. Of course, if you want guys to watch movies, what kind of movies are you going to advertise.
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Pediatrics. 2004 Dec;114(6):e694-8.
Unsafe and violent behavior in commercials aired during televised major sporting events.Tamburro RF, Gordon PL, D'Apolito JP, Howard SC.Division of Critical Care Medicine, St Jude Children's Research Hospital, and Le Bonheur Children's Medical Center, 332 North Lauderdale, Memphis, Tennessee 38105-2784, USA. robert.tamburro@stjude.org… For sporting events with >3 programs in the top 50 (NFL regular season games, NFL playoff games, Winter Olympic events, and Major League Baseball World Series)…commercials … were reviewed at standard speed for unsafe behavior or violence. …Commercials were categorized according to the product being advertised. Unsafe behavior was simply defined as any action that could have harmful consequences or that contravened the injury prevention recommendations of national organizations. ... The proportion of commercials that depicted unsafe behavior and/or violence during each sporting event was compared with the proportion of such commercials that were observed during the Masters Golf Tournament (which had the lowest proportion of commercials depicting such behavior). The proportion of commercials that contained violent/unsafe behavior for each advertised product was compared with the proportion of such commercials that advertised food or nonalcoholic beverages…. Of the 1185 commercials assessed, 14% (n = 165) displayed unsafe behavior and 6% (n = 66) depicted violence. Of the 322 commercial breaks, 158 (49%) contained at least 1 commercial showing unsafe behavior or violence. … The Super Bowl had the highest proportion of such commercials, and the Masters Golf Tournament had the least (relative risk: 4.3; 95% confidence interval: 1.4-12.5). The Masters Golf Tournament was noteworthy for the complete absence of violent commercials. Only 18% of reviewed commercials advertised movies or television programs, yet these commercials accounted for 86% of all violent commercials. Forty-eight percent of commercials that contained violence were for movies, and an additional 38% were for television programs. … Several categories of commercials portrayed unsafe behaviors; commercials for automobiles accounted for the most. In 8 different categories, 10% or more of the commercials depicted unsafe behavior, …
Tuesday, October 04, 2005
Association of Risk Factors for Breast Cancer with Types of Work
Another paper observes that physical activity at work protects women against breast cancer. This implies a healthier worker effect for breast cancer among women whose work activities are in factories with notable chemical exposures.
It’s well established that women in “professional” jobs are at increased risk compared to those who are not. Social class and education confound with other “lifestyle” issues like age at first childbirth, diet, time to exercise outside of work. BrooklynDodger hopes for a quantitative measure of the metabolic activity of various kinds of work, and a distribution of this activity by occupational class.
This study finds the effect most prominent in older than younger women. This is a very small study, so this may be a size effect.
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Kruk, J. and Aboul-Enein, H. Y.
Occupational physical activity and the risk of breast cancer.
Cancer Detect Prev. 2003; 27(3):187-92.
The association between occupational and the risk of breast cancer was analyzed using data from a case-control study of 257 women with breast cancer and 565 control women. After adjusted for potential confounders, women in sedentary occupations had a 29% higher risk, compared to those with the physically medium demanding jobs. For women at age > or =55 years higher occupational physical levels were associated with 53-60% reduction in the risk. There was a significant decreasing trend in the ORs from sedentary to medium work (P=0.001); while no association emerged in younger women.
It’s well established that women in “professional” jobs are at increased risk compared to those who are not. Social class and education confound with other “lifestyle” issues like age at first childbirth, diet, time to exercise outside of work. BrooklynDodger hopes for a quantitative measure of the metabolic activity of various kinds of work, and a distribution of this activity by occupational class.
This study finds the effect most prominent in older than younger women. This is a very small study, so this may be a size effect.
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Kruk, J. and Aboul-Enein, H. Y.
Occupational physical activity and the risk of breast cancer.
Cancer Detect Prev. 2003; 27(3):187-92.
The association between occupational and the risk of breast cancer was analyzed using data from a case-control study of 257 women with breast cancer and 565 control women. After adjusted for potential confounders, women in sedentary occupations had a 29% higher risk, compared to those with the physically medium demanding jobs. For women at age > or =55 years higher occupational physical levels were associated with 53-60% reduction in the risk. There was a significant decreasing trend in the ORs from sedentary to medium work (P=0.001); while no association emerged in younger women.
Workplace violence in Health Care Settings
Workplace violence is a major health and safety problem to service workers, especially health care workers. Management forces cite the incidence of injury from violence, to justify concentrating on co-worker assaults, and advancing profiling. The paper abstracted below shows that client violence is more important to social service and health care workers.
The main finding from this survey of Minnesota nurses was that workplace violence victims were far more likely than non victims to be in nursing homes, geriatric care and long term care environments.
BrooklynDodger looked at the full text long enough to be confident that “zero tolerance policy” – the lead preventive measure, was not defined. Maybe it’s a term of art in the health care community.
In order to decipher these results, we’d need to see the prevention measures stratified by work environment.
Extract from full text:
“Nurses were asked about eight different policy components: ‘‘Prior to (specific month), did your facility/institution/agency have a written policy on violence that addressed any of the following: (a) ‘zero tolerance’ for violence, that is, violence was not tolerated at any level; (b) types of violent behaviours (physical assault, threat, sexual harassment, or verbal abuse) that were prohibited; (c) consequences for those who used violence at work; (d) how to report if someone sexually harassed, threatened, or verbally abused you; (e) how to report if someone physically assaulted you; (f) assurance that reporting of violent incidents would be kept confidential; (g) requirements for violence prevention training of staff members; and (h) requirements for flagging of charts or other signals to staff members regarding patients/clients with repeated violent behaviour?’’ Response options included yes, no, and unsure. They were then asked the degree to which policy components were enforced.”
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Relation between policies and work related assault: Minnesota Nurses’ Study
N M Nachreiner, S G Gerberich, P M McGovern, T R Church, H E Hansen, M S Geisser, A D Ryan
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
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Occup Environ Med 2005;62:675–681
…From Phase 1 of the Minnesota Nurses’ Study, a population based survey of 6300 Minnesota nurses (response 79%), 13.2% reported experiencing work related physical assault in the past year. In Phase 2, a case-control study, 1900 nurses (response 75%) were questioned about exposures relevant to violence, including eight work related violence prevention policy items. … Results of multiple regression analyses, controlling for appropriate factors, indicated that the odds of physical assault decreased for having a zero tolerance policy … and having policies regarding types of prohibited violent behaviours … Analyses adjusted for non-response and non-selection resulted in wider confidence intervals, but no substantial change in effect estimates….
The main finding from this survey of Minnesota nurses was that workplace violence victims were far more likely than non victims to be in nursing homes, geriatric care and long term care environments.
BrooklynDodger looked at the full text long enough to be confident that “zero tolerance policy” – the lead preventive measure, was not defined. Maybe it’s a term of art in the health care community.
In order to decipher these results, we’d need to see the prevention measures stratified by work environment.
Extract from full text:
“Nurses were asked about eight different policy components: ‘‘Prior to (specific month), did your facility/institution/agency have a written policy on violence that addressed any of the following: (a) ‘zero tolerance’ for violence, that is, violence was not tolerated at any level; (b) types of violent behaviours (physical assault, threat, sexual harassment, or verbal abuse) that were prohibited; (c) consequences for those who used violence at work; (d) how to report if someone sexually harassed, threatened, or verbally abused you; (e) how to report if someone physically assaulted you; (f) assurance that reporting of violent incidents would be kept confidential; (g) requirements for violence prevention training of staff members; and (h) requirements for flagging of charts or other signals to staff members regarding patients/clients with repeated violent behaviour?’’ Response options included yes, no, and unsure. They were then asked the degree to which policy components were enforced.”
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Relation between policies and work related assault: Minnesota Nurses’ Study
N M Nachreiner, S G Gerberich, P M McGovern, T R Church, H E Hansen, M S Geisser, A D Ryan
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
. . . . . . . . . . . . . . . . . . . . . . .
Occup Environ Med 2005;62:675–681
…From Phase 1 of the Minnesota Nurses’ Study, a population based survey of 6300 Minnesota nurses (response 79%), 13.2% reported experiencing work related physical assault in the past year. In Phase 2, a case-control study, 1900 nurses (response 75%) were questioned about exposures relevant to violence, including eight work related violence prevention policy items. … Results of multiple regression analyses, controlling for appropriate factors, indicated that the odds of physical assault decreased for having a zero tolerance policy … and having policies regarding types of prohibited violent behaviours … Analyses adjusted for non-response and non-selection resulted in wider confidence intervals, but no substantial change in effect estimates….
Monday, October 03, 2005
Another WTC follow up study - Health Effects Incident After Exposure Ceased
BrooklynDodger keeps returning to WTC health effects for the lessons learned. The WTC event created a data base of health effects among workers who were at the site. Dodger has repeatedly pointed out that all measures of exposure on the ground were in compliance, well in compliance with OSHA standards. At various times there might have been high exposures to large particle dusts – greater than 10 micron – which are excluded by OSHA sampling methods and which may have been responsible for some of the health effects observed. But there is not a reason to believe the exposures after the first day were quantitatively or qualitatively that much different than a fire, building collapse or demolition that could happen anywhere. The difference was likely duration of exposure for response and construction personnel on the site.
This paper is only in abstract, likely a meeting presentation. Authors are based in Pennsylvania, so it’s yet another research group, different from Mt. Sinai, NYU or Johns Hopkins.
The Dodger can’t tell you what the high, medium or low exposure groups were, or the general exposure period or duration. However, as police officers they were unlikely to be using powered equipment to generate dust, or welding fume.
The observation was that respiratory symptoms got worse between October 2001 and 18 months later. Wheezing, phlegm and shortness of breath increased markedly compared to cough. Frequency was alarmingly high. Response bias is an issue, but it’s hard to see how the exposure response relationship would have emerged from response bias.
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Annals of Epidemiology Volume 15, Issue 8 , September 2005, Page 662 Abstract
Evolution of respiratory symptoms in New York Police Officers over eighteen months post 9/11
L.V. Buyantseva, G. Kampala, G. Leticia, Z.M. Ian, L.L. Engle, R. Gillis, A. Roberts and R. Bosom Penn State College of Medicine, Hershey, PA
Respiratory symptoms have emerged as the most common physical sequel in 9/11 first responders. We assessed evolution of those symptoms over eighteen months in New York Police Officers…
Initial survey (IS) in October 2001 included 1587 Hypos. 575 (36%) agreed to answer the follow-up survey (FUS) eighteen months later. NYPOs 9/11 exposure categories were: light (n = 69), moderate (n = 174) and high (n = 228) [category was not assigned in 70 participants]…. Cough was the most common symptom reported by 43.5% and 43.5% of all officers at IS and FUS (p = 0.7), respectively. Occurrence within exposure groups in the order of severity was 24.6%, 42.5%, and 50% (p < 0.0001) on IS; and 30.9%, 43.7%, and 47.1% (p = 0.059) on FUS. Wheezing was reported by 13.1% and 25.9% on IS and FUS (p < 0.0001), respectively. Its frequency in exposure brackets was 3%, 14.6%, and 15% (p = 0.02) on IS, while increasing to 14.5%, 25.9%, and 29.4% (p = 0.05) on FUS. Phlegm was reported by 14.4% and 67% on IS and FUS (p < 0.0001), respectively. Its frequency in exposure brackets was 1.5%, 13.8%, and 18.9% (p = 0.001) on IS; and 21%, 35.3%, and 30.2% (p = 0.1) on FUS. Shortness of breath (SOB) was reported by 18.9% and 43.6% on IS and FUS (p < 0.0001), respectively. Its frequency in exposure brackets was 10.1%, 13.8%, and 25.4% (p = 0.002) on IS and 31.9%, 45.1%, and 46% (p = 0.1) on FUS. Analysis against risk factors showed that none of the symptoms at eighteen months could be attributed to smoking, and only SOB reported at IS was modified by the use of respiratory protection.
Conclusions
While cough remained the most common and stable respiratory symptom, there was a significant increase in phlegm, wheezing and shortness of breath. This observation raises concern that respiratory injury may have progressed over time and requires further monitoring.
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Sunday, October 02, 2005
Taking the Work Organization Bait, Falling into the Psychosocial Trap
Another Annals abstract, likely a meeting presentation. A very distinguished group of investigators take the work organization bait and fall into the psychosocial causes of MSD trap.
Plus, they publish the relative risks and never give you an anchor, so a public health authority has no reference rate for prevalence.
The problem is, if piece work causes carpal tunnel syndrome, what are you going to do about that? Plus, if stress causes this physical ailment, or symptoms complaints, then mechanical interventions such as OSHA can order don’t mean much. Where’s your biological plausibility? Just hire happy workers, or train them how to cope. Gene Scalia frequently argued that CTS or whatever was all in the workers’ head.
The problem is, if there is a narrow range of exposure to risk factors in your population, then host factors dominate in the model. If there were no difference in ergo risk factors in the population, then ergo risk factors would disappear from the model.
The next problem is that the job content questionnaire is not appropriate [sucks?] when applied to factory work. The Dodger has read the questions, they are mostly subjective responses of the employee to the work environment, not observable and not meaningful especially for assembly line work.
In the Dodger’s real world of summer jobs experience, there’s not much difference between the basics of sewing machine operators in small shop sewing jobs. Except, there are a couple of ?safety stitch machine operators [not sure the Dodger actually remembers the name right, machine sews the seam and cuts the excess material] on piecework who go like bats. This is the high skilled job assembling the garment, maybe for shirts these are single or double needle machines. These people can make money on piece rates, and feed the whole line downstream. You aren’t going to move them off their machine. If their machine goes down, they are distinctly unhappy. There’s a variety of other machines, like the bar tack [where belt loops are put down] where nobody much can beat the rate and which are substantially lower skilled.
So this confounds working on one machine, piece work, repetitiveness, plus maybe a more forceful pinch grip controlling the tension when feeding the machine.
This study would be much more likely to demonstrate risk factors if pressers or the floor workers were included. They have little or no repetitive upper extremity work, even if some back injury risk and walking and standing risks.
Plus, they publish the relative risks and never give you an anchor, so a public health authority has no reference rate for prevalence.
The problem is, if piece work causes carpal tunnel syndrome, what are you going to do about that? Plus, if stress causes this physical ailment, or symptoms complaints, then mechanical interventions such as OSHA can order don’t mean much. Where’s your biological plausibility? Just hire happy workers, or train them how to cope. Gene Scalia frequently argued that CTS or whatever was all in the workers’ head.
The problem is, if there is a narrow range of exposure to risk factors in your population, then host factors dominate in the model. If there were no difference in ergo risk factors in the population, then ergo risk factors would disappear from the model.
The next problem is that the job content questionnaire is not appropriate [sucks?] when applied to factory work. The Dodger has read the questions, they are mostly subjective responses of the employee to the work environment, not observable and not meaningful especially for assembly line work.
In the Dodger’s real world of summer jobs experience, there’s not much difference between the basics of sewing machine operators in small shop sewing jobs. Except, there are a couple of ?safety stitch machine operators [not sure the Dodger actually remembers the name right, machine sews the seam and cuts the excess material] on piecework who go like bats. This is the high skilled job assembling the garment, maybe for shirts these are single or double needle machines. These people can make money on piece rates, and feed the whole line downstream. You aren’t going to move them off their machine. If their machine goes down, they are distinctly unhappy. There’s a variety of other machines, like the bar tack [where belt loops are put down] where nobody much can beat the rate and which are substantially lower skilled.
So this confounds working on one machine, piece work, repetitiveness, plus maybe a more forceful pinch grip controlling the tension when feeding the machine.
This study would be much more likely to demonstrate risk factors if pressers or the floor workers were included. They have little or no repetitive upper extremity work, even if some back injury risk and walking and standing risks.
A useful reanalysis of this work would be a matrix showing the association of piece rate with the physical risks.
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Annals of Epidemiology Volume 15, Issue 8 , September 2005, Page 655
Work organization and work-related musculoskeletal disorders for sewing machine operators in garment industry
P.C. Wang1, B. Ritz1, D. Rempel2, R. Harrison3, J. Chan3 and I. Janowitz2 1Department of Epidemiology, University of Los Angeles, Los Angeles, CA2University of San Francisco/Berkeley Ergonomics Laboratory, Richmond, CA3California Department of Health Services, Oakland, CA …
We recruited 314 Hispanic and Chinese sewing machine operators from 12 garment shops in Los Angeles, California from 2003 to 2004. Data were collected through physical exams and standardized interviews. Cases are defined as workers reporting pain at least one day per week with a pain score higher than 2 out of 5 during a 1-month period. Symptoms were assessed by anatomical regions and are summarized here as pain in neck/shoulder, back/hips, upper or lower extremity.
Results
We found that pain symptoms were reported more often by workers who were paid via a piece rate … (In neck/shoulders adjusted odds ratio (aOR) = 2.25; 95% confidence interval (CI): 1.1–4.8; in back/hips aOR = 2.54; 95%CI: 1.3–5.2; in upper extremity aOR = 2.94; 95%CI: 1.1–8.0; in lower extremity aOR = 2.69; 95%CI: 1.0–7.4), and who work on monotonous and repetitive work such as single machine users especially for pain in back/hips (aOR = 2.30; 95% CI: 1.1–4.7). Low decision authority was associated with an increased risk of reporting pain in upper extremity (aOR = 2.87; 95%CI: 1.1–7.6) and back/hips (aOR = 2.31; 95%CI: 1.0–5.2). High psychological job demand was associated with an increased risk of reporting pain in upper extremity (aOR = 2.07; 95%CI: 1.0–4.1). An exposure-response trend was observed for physical exertion and pain in four body sections, and physical isometric loads above the mean increased neck/shoulders and lower extremity pain.
Conclusion Our results suggest that work organizational factors are associated with an increased risk of reporting WRMDs in sewing machine operators.
Saturday, October 01, 2005
More on Breast Cancer and Work
BrooklynDodger continues the series on breast cancer and work. A previous post found the protective effect of physical activity was most prominent in older women. This paper observes the effect to be more prominent in younger women. When risks were adjusted for social class, the protective effect of physical activity was attenuated. BrooklynDodger suspects this is because increased physical activity at work is associated with lower social class. All this defaults to the distribution of risk factors among the Finnish population.
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Rintala, P. E.; Pukkala, E.; Paakkulainen, H. T., and Vihko, V. J.
Self-experienced physical workload and risk of breast cancer.
Scand J Work Environ Health. 2002 Jun; 28(3):158-62.
Occupational physical activity was estimated from a self-determined rating [scale 1 (low)-5 (high)] of occupational physical load for 1800 randomly selected women born in 1930-1969. …Occupation-specific numbers of observed and expected cases of breast cancer … were grouped according to the index for occupational physical activity. Expected rates were calculated with the social-class-specific population and the entire Finnish female population as reference populations. The relative risks (RR) of breast cancer for categories 3-5, in comparison with categories 1-2 were calculated … The RR was lower for occupations in category 5 than for those in categories 1-4, especially in the youngest (25-39 years) age group (RR 0.51…). …
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Rintala, P. E.; Pukkala, E.; Paakkulainen, H. T., and Vihko, V. J.
Self-experienced physical workload and risk of breast cancer.
Scand J Work Environ Health. 2002 Jun; 28(3):158-62.
Occupational physical activity was estimated from a self-determined rating [scale 1 (low)-5 (high)] of occupational physical load for 1800 randomly selected women born in 1930-1969. …Occupation-specific numbers of observed and expected cases of breast cancer … were grouped according to the index for occupational physical activity. Expected rates were calculated with the social-class-specific population and the entire Finnish female population as reference populations. The relative risks (RR) of breast cancer for categories 3-5, in comparison with categories 1-2 were calculated … The RR was lower for occupations in category 5 than for those in categories 1-4, especially in the youngest (25-39 years) age group (RR 0.51…). …
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