More Piling On: Obesity Association with Injury Risk Equivocal

Am J Prev Med 2005;29(1): 41–45
Obesity and Risk of Nonfatal Unintentional Injuries

Huiyun Xiang, MD, MPH, PhD, Gary A. Smith, MD, DrPH, J. R. Wilkins III, BCE, DrPH,
Guanmin Chen, MD, PhD, Sarah Grim Hostetler, BA, Lorann Stallones, MPH, PhD

Background: Obesity is recognized as a risk factor for multiple chronic diseases. Yet, it is unclear whether
obesity is also associated with an increased risk of nonfatal unintentional injury.

Methods: A population-based survey was conducted among adults aged
18 years from January 1999
through October 2000. The relationship was investigated between body mass index (BMI),
defined as weight in kilograms divided by the square of the height in meters (kg/m2), and
risk of nonfatal unintentional injuries among 2575 respondents aged
20 years by
comparing percentage of adults between obese and nonobese respondents who had
injuries. Multivariate logistic regression further examined this relationship by controlling
for confounding demographics.

Results: A total of 370 respondents reported injuries in the previous year. We observed a linear
dose–response trend among women. An estimated 7.0% of underweight individuals (BMI

18.5) reported injuries. In contrast, 26.0% of men and 21.7% of women with a BMI
35.0
reported injuries. The odds ratio of injuries for individuals with a BMI
35.0 was 2.00 (95%
confidence interval1.07–3.74, p
0.05) after controlling for gender, age, education level,
marital status, family poverty status, and area of residence.

Conclusions: A marginally significant association between extreme obesity and elevated risk of injuries
was observed. Efforts to promote optimal body weight may reduce not only the risk of
chronic diseases but also the risk of unintentional injury among overweight and obese
individuals.

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BrooklynDodger Comments: Basically, this study provides only equivocal evidence for increased injury risk associated with increased BMI, and that mostly in women. A risk ratio of 2 is pretty strong, driven by MSD's, but two adjustments were needed to the model to get marginal statistical significance.

This population survey observed that 14% of respondants suffered an injury requiring greater than first aid treatment. Only 2% of respondents confessed being very obese. A BMI of 35 in a 6 foot tall person is a weight of 258, which is undersized for an NFL linebacker... The Dodger is no fan of overweight, but also no fan of the trend to blame victims as a softening up process for cutting health care benefits.

The survey observed that about 35% of injuries occurred at work. Considering maybe 40% of waking hours are at work, and less than 100% of the respondents were economically active [actual number not found by BD, maybe not asked], work is riskier than not working for injury. About 35% of injuries were over exertion [that is, MSD's]; these were the only category where the obese were higher than the non obese.

An association of overweight with back injury has a biomechanical plausibility. The increase might also arise from a common driver of health risk behavior [over eat] with injury risk behavior.

The investigators give us two weasel words, "suggest" and "may" in their conclusion: "The findings suggest that efforts to promote optimal body weight may reduce not only the risk of chronic diseases but also the risk of nonfatal unintentional injuries among obese individuals."

Climate Change and the Precautionary Principle

Risk Analysis Volume 25 Page 1399 - December 2005

Volume 25 Issue 6

Defining Dangerous Anthropogenic Interference: The Role of Science, the Limits of Science

Michael Oppenheimer*

Defining "dangerous anthropogenic interference with the climate system" in the context of Article 2 of the UN Framework Convention on Climate Change (UNFCCC) presents a complex challenge for those developing long-term climate policy. Natural science has a key role to play in quantifying vulnerabilities of elements of the Earth system and estimating the risks from a changing climate. But attempts to interpret Article 2 will inevitably draw on understanding from social science, psychology, law, and ethics. Here I consider the limits of science in defining climate "danger" by focusing on the potential disintegration of the major ice sheets as an example of an extreme impact. I show that considerations of timescale, uncertainty, and learning preclude a definition of danger drawn purely from natural science. Decisionmakers will be particularly challenged by one characteristic of global problems: answers to some scientific questions become less accurate over decadal timescales, meandering toward the wrong answer, a feature I call negative learning. I argue for a precautionary approach to Article 2 that would be based initially on current, limited scientific understanding of the future of the ice sheet. >>>>>>>>>>>>>>>>>>>>>>>>>>> BrooklynDodger comments: The Dodger hasn't been a fan of the precautionary principle, applied to occupational safety and health issues. For leading occupational issues, "decisionmaking in the face of uncertainty," is a false paradigm, what's really happening is refusal to act in the face of certainty. For example, the refusal to address poorly soluble particles with low toxicity in the occupational environment, following the wave of community studies. However, the Dodger concedes a continuum of precautiousness. At one end, if there's two bioassays, mechanistic information, and clear evidence of carcinogenicity in humans, there's sometimes a choice of model for high to low dose extrapolation. At the other end are persistent organic pollutants, where human health effects are thinly documented in the community and marginal in occupational setting [dioxin] but typically consistent with risks predicted from laboratory studies. The Dodger is impressed that somewhere on the other end is the debate over Genetically Modified crops, mostly an EU debate. Here there's little data for risk, other than fear of "messing with mother nature." [Although the defense of GMO is often a depiction of the damage done by non modified invasive species, which hardly reassures.] The GMO debate over precaution is somewhere in the area of "whether" there is a risk, almost at the level of hazard identification. Climate change is more about "how big" and "when" Anyway, Risk Analysis publishes about a 1:10 ratio of precaution to corporatist briefs. The paper cited above relays thoughts about doing something about global climate change which never quite reach a conclusion. Somewhere in the middle of th paper, Oppenheimer states a question but doesn't give an answer: The example of the ice sheets demonstrates three points: (1) the impact of ice sheet disintegration would be very large; (2) the risk from global warming cannot be quantitatively estimated as a function of local polar temperature because there is no ice sheet model that reproduces recent changes in the ice, and because the relation of local to global temperature changes is very uncertain; and (3) timescales over which disintegration may occur could be so long as to be irrelevant to most people, or could be short enough to make adaptation to resulting sea level rise very difficult. Uncertainties inherent in point (2) with regard to what amount of warming could trigger disintegration are so large that one approach that might seem reasonable to some people involves ignoring the problem altogether until understanding increases. Others would view the risk as demanding preemptive action despite the uncertainties. Similarly, the uncertainties in timing are so large that a range of judgments could be anticipated. The Dodger muses that climate change is mostly an economic impact, with health effects secondary to economic changes. Warming means more water in the ocean, heavily impacting where people live now, more rain falling on land but in different places than it is now.

The Ultimatum in Labor Negotiations

Game theory and behavioral economics is scientific enough to bring this to the Dodger's blog.

The ultimatum game should caution an employer in a dominant position, like Delphi is these days. It should caution an occupying power, like the US in Iraq.

Basically, the dominant player offers a division of the reward to the second player in a single transaction game. In the case above, the first player offers 2 to the second, keeping 8. If the second player refuses, both get nothing. From the second player's perspective, even a penny is better than nothing. However, when the game is played in the laboratory, the second player rejects low offers frequently, and the first player offers substantial amounts, like 3 to 5 points.

Game theorists speculate why. The Dodger thinks it's because people react like it's a multiple interaction game rather than a single transaction, because that's life. In real life you can never be sure you will never see the other guy again, or that he won't see you and screw you again.

Let's take the situation with Delphi. Say Delphi offers to pay $1.00 over market wage. If the workers reject, their alternative is to go out on strike and maybe kill the company, in which case they go out and get a market wage job, and give up the dollar. Which they may well do, if the offer is too much of an ultimatum.

The important calculation is how much worse off will the Delphi executives who are making abusive offers be if they blow up Delphi and sink GM. If they aren't any worse off, why should they care?



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http://en.wikipedia.org/wiki/Ultimatum_game

Ultimatum game
From Wikipedia, the free encyclopedia.

The Ultimatum game is an experimental economics game in which two parties interact anonymously and only once, so reciprocation is not an issue. The first player proposes how to divide a sum of money with the second party. If the second player rejects this division, neither gets anything. If the second accepts, the first gets their demand and the second gets the rest.

Tautology and Intelligent Design

Scientists Find A DNA Change That Accounts For White Skin

By Rick Weiss
Washington Post Staff Writer
Friday, December 16, 2005; A01

Scientists said yesterday that they have discovered a tiny genetic mutation that largely explains the first appearance of white skin in humans tens of thousands of years ago, a finding that helps solve one of biology's most enduring mysteries and illuminates one of humanity's greatest sources of strife.

...

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BrooklynDodger Comments: The Dodger's first bounce on this paragraph was "What other kinds of mutation are there besides genetic mutations?" The, the pedant in the Dodger thought that WaPo might have been trying to distinguish a germline mutation from a somatic mutation. The Dodger also wondered whether there's gene silencing which has the same effect.

The investigators noted the mutation in non-striped Zebrafish, and a similar "tiny" [single nucleotide polymorphism, SNP?] in people. Evidence for common descent going back before the radiation of fishes from the lines which became people.

ID a, nd creationism are making their big splash just at the time that the underlying mechanisms for evolution by natural selection are strenthening.

The Dodger further notes that DNA, or the alternative intitial replicator, can't be the product of the Intelligent Designer setting a clockwork of life on earth into motion. There can only be one big bang, supernatural in the sense of no ability to have natural knowledge, starting the universe into motion. There's no role for a the Designer coming back for a second biological big bang.

[PS: The eye has evolved, in different forms, dozens of times. Perhaps the ballot official illustrated above is another.]

Popcorn Workers Lung (IV)

BrooklynDodger thinks this is the fifth in the series of NIOSH papers on popcorn workers lung. The Dodger sympathizes with the investigators trying to characterize a never before seen association between lung disease and exposure to a "safe" food additive.

The Dodger notes again that nothing is visible regarding surveillance of workers at sites other than than the index site, that there is no visible chronic or subchronic bioassay of diacetyl, the most strongly suspected chemical agent, and there is no exposure guideline recommended, much less promulgated as a standard.

BrooklynDodger has been told there's some gray literature on this, such as data on exposures from consumer applications of butter flavoring.

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Chest. 2005 Aug;128(2):991-7.

Induced sputum evaluation in microwave popcorn production workers.

Akpinar-Elci M, Stemple KJ, Enright PL, Fahy JV, Bledsoe TA, Kreiss K, Weissman DN.
NIOSH Division of Respiratory Diseases Studies, Centers for Disease Control and Prevention/National Institute for Occupational Safety and Health, Field Studies Branch, Mail Stop H-2800, 1095 Willowdale Rd, Morgantown, WV 26505, USA. melci@cdc.gov

OBJECTIVE: Severe airways obstruction and bronchiolitis obliterans have been reported in microwave popcorn production workers and attributed to inhalation of flavoring agents. We investigated whether exposure to flavoring agents is associated with airways inflammation in popcorn production workers.

METHODS: Fifty-nine workers with high exposures and 22 patients with low exposures to flavoring vapors completed a questionnaire, spirometry, and sputum induction. Sputum cell counts were categorized as "high" if greater than (and "low" if less than or equal to) the median cell counts of a healthy external control group (n = 24). We compared high- and low-exposure groups as well as all workers with control subjects.

RESULTS: Neutrophil concentrations in nonsmoking workers were significantly higher than those of the healthy nonsmoking control group (p <> 1.63 x 10(5)/mL) was 3.8 (95% confidence interval, 1.3 to 11.5) in the high-exposure group compared with the low-exposure group. Sputum interleukin-8 and eosinophil cationic protein levels were higher in high-exposure workers than in low-exposure workers (p <> 95%. There were no relationships between sputum characteristics and the presence of airways obstruction.

CONCLUSIONS: High exposure to popcorn flavoring agents is associated with neutrophilic airway inflammation in popcorn production workers. These data provide further evidence that popcorn production workers face a significant occupational hazard through exposure to flavoring agents.

EPA Particle Rules and Occupational Exposures

EPA announced its new proposed particle air quality standards. These were promptly denounced as too weak, allowing too much exposure, and contrary to the Clean Air Science Advisory Committee recommendations. BrooklynDodger will post about those scientific issues later. Let's just say that even George W. Bush thinks these standards are needed.

[Mike Leavitt, EPA administrator trained for this public health post as Governor of Utah. Historically, the first major modern study demonstrating adverse effects of particles at these levels was done in Utah. The Dodger posted on this previously.]

In short, these standards are supported by lots of epidemiology that shows increases in death, and hospitalization from respiratory and cardiac causes from fluctuations in particle levels within the range permitted by present and these proposed EPA limits. And despite canonical references to old sick people and children, it isn't only them who are effected.

EPA summarizes the proposal:

"Fine particles - 24-hour standard

• An area would meet the 24-hour standard if the 98th percentile of 24-hour PM2.5 concentrations in a year, averaged over three years, is less than or equal to the level of the standard EPA sets in its final rule (35µg/m3 under this proposal). This is the same form as the current 24-hour standard.

Fine particles – annual standard

• An area would be in compliance with the annual PM2.5 standard when the three-year average of the annual average PM2.5 concentration is less than or equal to 15 µg/m3 (or whatever level of standard EPA sets in its final rule). This is the same form as the current annual standard.

• Current fine particle standards allow some areas to average measurements from multiple community-oriented monitors to determine compliance with the annual standard. The proposed revisions also would limit the conditions under which this averaging could take place. EPA also is seeking public comment on no longer allowing averaging measurements from multiple community monitors. Inhalable coarse particles

• An area would meet the coarse particle standard if the 98th percentile of 24-hour PM10-2.5 concentrations in a year, averaged over three years, is less than or equal to the level set in the final rule (70µg/m3 in this proposal). This form will provide a more stable target for air pollution control programs by reducing the impact of unusual weather conditions, such as high wind events.
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BrooklynDodger comments: Ok, figure "fine" particles (PM 2.5) essentially the same as OSHA respirable [Count distribution would vary based on source; fine particles in environment tend to be agglomeration of combustion ultrafines, some manufacturing processes are energetic enough to mechanically generate some bigger smaller particles]. And "coarse" particles (PM 2.5 - PM 10) are essentially the same as OSHA total. [OSHA total closed face filter and the EPA method cut off larger particles, which have a lot of mass but little of particle count.]

The 98th percentile deal on daily average means 7 or 8 days a years can exceed the limit before the area gets busted for violating the rule.

How would we convert these values into occupational levels of concern? Let's say that half the air a worker breathes is breathed at work. That's conservative, since about 40% of waking hours are at work, but people breath a lot more at work than at leisure, and lot more awake than asleep.

For respirable particles, the proposal would translate to 70 micrograms six days a year, [ok, 100], and 30 micrograms averaged over the year. [Should be added to the community level for health protection.]

For total particulate, the proposal would translate to 140 micrograms, 6 days a year. Outside of grinding or sanding operations, it's likely most of total is really respirable or smaller.

Mold Remediation Ventilation

BrooklynDodger comments: The Dodger recently mused on protective schemes for airborne aerosol biologic agent exposure, with emphasis on Katrina related mold. [The Dodger believes this is the first internal reference to a BrooklynDodger blog posting.]

Mold remediations these flooded homes, or restorations in general, are "just" remodeling projects in small homes. Obvious protections are basic construction standards. Those standards require a competent person and training in hazards for all employees, although these general standards are rarely enforced by OSHA. The most convenient way to deliver these requirements would be a 30-hour construction card for the supervisor and 10-hour cards for the workers. Dream on.

But there are specifics where mold is being disturbed, which under the plain language of HAZWOPER should be covered by the standard.

The Dodger notes lack of recommendations for ventilation during mold remediation or other construction projects.

Let's imagine a room 20 ft x 50 ft with a 10 ft ceiling, which could maybe be a floor of a small house. Thus, 1000 sq ft and 10,000 cf. The Dodger measured the exhaust volume of a $15.00 [on sale at hardware store], 20 inch square window fan at 1000 to 2000 cfm; they move surprising amount of air against no static pressure. Thus, 1 cfm/sq foot and a 10% volume/minute replacement rate, or 6 air changes per hour minimum [yes, the Dodger knows air changes per hour is dislike terminology.]

[Houses have less volume per outside dimensions because the ceilings aren't usually that high, and interior volume is taken up by walls and other structures.]

[By contrast, a modern air conditioned office is designed for 1 air change, but it's mostly recirculated air.]

The 6 air changes is better than most factories have for general air. The fan would have to be framed into an open window with duck tape and cardboard. If you wanted better ventilation, you could spring for two, the cardboard with lying around and there's plenty of tape left on the roll. [Square shape of the housing is a benefit here, it would be require more crafting for a round fan.]

The point here is that lots of exposure is aerosol hanging in the air; mold spores may be generated continuously by the fruiting bodies, but dust is not being generated continuously, and the fan could clear them out and reduce reliance or improve effectiveness of a respiratory protection scheme. Workers standing parallel to the general flow of air would get some additional protection.

The fan is only generating about 5 fpm through the plane of the 10 x 20 short axis of the room, but would be generating upwards of 100 fpm through a doorway, which would certainly contain dust within a room. Plastic sheeting in the door would increase containment.

The Dodger applied this scheme during floor resurfacing in the Dodger's home. It worked great until the resurfacers, not understanding, turned off the fan.

The difference between mold remediation aerosol and asbestos remediation aerosol is that mold particles are less durable, and found in the environment anyway [that's how they got to seed the inside of the building to begin with.] Those who wish containment could tape a HEPA furnace filter to the back of the fan, which would cost some volume.

Fat and Happy, Maybe Not Dumb

American Journal of Epidemiology 2006 163(1):1-8;

Original Contribution

Association of Body Mass Index with Suicide Mortality: A Prospective Cohort Study of More than One Million Men

Patrik K. E. Magnusson¹, Finn Rasmussen^2,3, Debbie A. Lawlor⁴, Per Tynelius^2,3 and David Gunnell⁴

¹ Department of Genetics and Pathology, Uppsala University, Uppsala, Sweden
² Child and Adolescent Public Health Epidemiology Group, Department of Public Health Sciences, Karolinska Institute, Stockholm, Sweden
³ Division of Epidemiology, Stockholm Centre of Public Health, Stockholm, Sweden
⁴ Department of Social Medicine, University of Bristol, Bristol, United Kingdom

Correspondence to Dr. Finn Rasmussen, Child and Adolescent Public Health Epidemiology Group, Department of Public Health Sciences, Karolinska Institute, Norrbacka, SE-171 76 Stockholm, Sweden (e-mail: finn.rasmussen@phs.ki.se).

The authors investigated the association of body mass index (BMI) with suicide in a record linkage study based on the Swedish Military Service Conscription Register, the Population and Housing Censuses, and the Cause of Death Register. The cohort studied consisted of 1,299,177 Swedish men who were conscripted in 1968–1999, had their BMI measured at age 18–19 years, and were followed up for as long as 31 years. A strong inverse association was found between BMI and suicide. For each 5-kg/m² increase in BMI, the risk of suicide decreased by 15% (95% confidence interval: 9, 21). The association was similar when subjects with mental disorder at baseline were excluded from the analysis. BMI-suicide associations were similar in relation to suicide deaths occurring in the first 5 years of follow-up (hazard ratio for each 5-kg/m² increase in BMI = 0.84, 95% confidence interval: 0.73, 0.96) compared with associations 10 years after baseline (hazard ratio = 0.87, 95% confidence interval: 0.79, 0.96), indicating that weight loss as a consequence of mental illness does not explain the BMI-suicide association and that factors influencing BMI may be causally implicated in the etiology of mental disorders leading to suicide.

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Brooklyn Dodger Comments: The Dodger's current framework on "personal" health is that stress causes mental illness causes risk behavior causes overweight, smoking, excessive drinking, bad driving, causes illness and death. Therefore, reading the title on medline, the Dodger thought for sure that obesity would be associated with suicide. To the Dodger's surprise, the conclusions went the other way.

Now to commentary on the paper. First, these are Swedes, thought to be gloomy and frequent suicide victims. Something for the Dodger to look up in the future.

Second, why did the authors and reviewers neglect to state the main outcome in the abstract? From the full text the Dodger gleaned: "1,299,177 men ... were included in this analysis.
Up to the end of 1999, a total of 3,075 (0.24 percent) died ... by suicide—the suicide rate measured from conscription was 16.2 per 100,000 per year."

Third, the only stratum signficantly worse that normal weight was underweight (bmi <> Since these BMI strata are arbitrary, the range of normal might be gerrymandered to make the benefits of "overweight" go away. For a 6-foot person, the upper boundry of underweight is 136 pounds, which is seriously thin. The upper bound of normal is 185 pounds, which is not seriously chubby.

Maybe the lower bmi stratum is poor in drinkers, and therefore at higher risk because of that?

Maybe the important finding is that obesity is not associated with increased suicide risk, and therefore whatever causes obsesity, or excessive eating, is not associated with increased suicide risk?

Framing Risk Assessment for Biological Agents and Carcinogens: What about mold?

Brooklyn Dodger Comments:

The Dodger grew up as a chemicals person. Chemicals are by no means "over." But the dangerous exposure of this year is mold inside Katrina-flooded houses in NOLA. What's the public health approach, and is there a way toward a quantitative exposure-based set of control measures?

"Biological" agents include infectious materials [TB, anthrax, SARS, flu], mold [spores], animal wastes [swine confinement, pigeons, bird droppings (which are infectious)], flour dust, pollen, and components of metalworking fluids. Biological agents share character with carcinogens, specifically, carcinogens in which aerosol exposure is the primary route.

Biological agents share with carcinogens the presumption of no practical threshold to the exposure-response relationship in an exposed [human] population. Absence of a practical threshold in a population may arise from a non-zero probability that a single organism or spore may give rise to infection. It may arise from an allergic [immune mediated] type of response, in which some population of pre-exposed and sensitized people will respond to vanishingly small doses. Or, there may be specially sensitive sub-populations without known pre-exposure.

Carcinogens threaten an irreversible increased risk of developing a progressive and potentially fatal condition after removal from exposure. That is, a future risk from past exposure. Effects of biological agents may also progress on removal; for example, an exposure triggered asthma condition may develop cross reaction to common community exposures and progressively damage the respiratory system.

For an individual, a "threshold" - the lowest exposure which will produce the effect - may be presumed, but it's of no practical use. The individual who suffers the effect was exposed above the individual's threshold [level, duration, schedule and latency], the individual who escapes was exposed below [or a censored by suffering an intervening alternative condition], but this can only be known after. The distribution of individual thresholds sums to the population exposure response relationship. The Dodger imagines there is a central tendency and dispersion of the probability of effect at each dose. BrooklynDodger imagines definable sub-populations [for example, some genetic marker for sensitivity, or some co-exposure] and variation in resistence in a single population.

Now, back to mold in buildings. The problem is there are unknowable numbers of species, sub species, varieties or whatever of mold. Unknowable means unmeasureable. Unmeasurable means no means of determining exposure-response. Molds fling spores into the air. There's mold stuff in the air all the time, everywhere, and there are people who suffer frequently, all the time [hay fever] and who take medicine all the time. They suffer more when their own private exposure is higher, and less when it's lower. Frequently a troubled building will have less measureable mold material in the air than outside, but its different mold.

There's some evidence that molds also produce vapor phase contaminants [3-methyl furan, or 3-MF] which have biological effect.

This handwaving suggests an explanation for people continuing to complain of symptoms after mold has been removed from a building - they are the sensitive or sensitized sub-population or people at the bottom of the exposure response curve. Assume for the sake of argument the building has an acceptable volume of acceptably cleaned air. Contrary to all the Dodger's ideals, these people need medicine, or respiratory protection, or else have to tough it out or leave.

The Dodger will futurely post on occupational health protections for mold remediation and other biological exposures.

Cat Scans on Persons with Indeterminate X-rays for Asbestos Disease

Int J Hyg Environ Health. 2005;208(1-2):87-99.

The usefulness of computed tomography in detecting asbestos-related pleural abnormalities in people who had indeterminate chest radiographs: the Libby, MT, experience.

Muravov OI, Kaye WE, Lewin M, Berkowitz Z, Lybarger JA, Campolucci SS, Parker JE.

Agency for Toxic Substances and Disease Registry, Atlanta, GA 30333, USA. oim0@cdc.gov

This epidemiological study was conducted to determine whether high-resolution computed tomography (HRCT) is useful to screen for pulmonary abnormalities in people exposed to vermiculite containing asbestos. During June-September 2001, we evaluated HRCT of 353 people in Libby, MT, who had been exposed to asbestiform minerals associated with vermiculite. Of these, 334 participants of the summer 2000 medical testing program underwent HRCT of the chest at St. John's Lutheran Hospital and 19 eligible people who recently had undergone an HRCT scan at the same facility and under the same testing protocol allowed the study reviewers to use that scan. All 353 study participants were former vermiculite mine/mill workers (n = 55), their household contacts (n = 99), and people exposed to vermiculite through recreational or other activities (n = 199). Participants' 2000 medical testing results indicated only one of the three B-reader chest radiograph reviewers had reported a pleural abnormality (indeterminate chest radiograph). Three expert computer tomography (CT) scan evaluators reviewed the HRCT scans and identified pleural abnormalities in 98 (27.8%) of the 353 participants whose previous chest radiographs were classified indeterminate. Of these 98 people, 69 (70.4%) were either former vermiculite mine/mill workers or household contacts, and 40 (40.8%) showed pleural calcification on HRCT. Thirty out of the 40 people with pleural calcification reported having no occupational exposure to either Libby vermiculite or asbestos. Our findings indicate that low-dose HRCT can be considered for screening certain former vermiculite mine/mill workers and their household contacts who have indeterminate chest radiographs and may be useful for diagnosing a suspicious finding on a chest radiograph, particularly in a high-risk person.

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BrooklynDodger comments: The Dodger was unable to access the full text of this paper. Among the big deals in the asbestos compensation battle is whether there are victims of asbestos with clean x-rays, or indeterminate x-rays. The abstract confuses. It would appear that 1 reader thought there was evidence on xray, but it's not clear what the 1/3 positive findings were.

Close only counts in horseshoes and hand grenades

Applied Ergonomics

Volume 37, Issue 2 , March 2006, Pages 113-118
Influence of hand grenade weight, shape and diameter on performance and subjective handling properties in relations to ergonomic design considerations

Cheng-Kang Yuan^{a, ,} and Cheng-Lang Kuo<sup>b,

a</sup>Department of Business Administration, Lunghwa University of Science & Technology, Taiwan, ROC
^bDepartment of Industry Management, China Institute of Technology, Taiwan, ROC

Received 8 September 2004; accepted 20 June 2005. Available online 15 August 2005.

Abstract

Three hand-grenade design factors, namely shape (ball, oval, can), diameter (55, 60, and 65 mm) and weight (300, 400, and 500 g), were assessed. The objective criteria were (1) throwing distance from the grenade stop point to throwing point, and (2) error distance from the grenade stop point to the target. The subjective criteria were (3) the overall rating of handling (to hold and control) properties and (4) the rating of perceived exertions of throwing strength. Twenty ROC Army soldiers threw a Mark II practice grenade to familiarize them with the throwing procedure, and then, while standing, threw 21 experimental, mockup grenades at a target indicated by a flagpole 40 m away from the throwing point. Grenade weight had the greatest effect on both subjective and objective criteria. The 300 g grenade had the greatest throwing distance (38.6±6.5 m) and had the greatest accuracy (6.9±3.9 m). Grenade shape was also a significant influence based on both the subjective and objective criteria; with the ball shape being the best. Grenade diameter, within the range tested, did not affect either the subjective or objective criteria.

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BrooklynDodger comments: Science marches on. Not that we don't need science applied to everyday life and death situations. In this case, it's a death situation suited to military planning.

The Dodger was not surprised that the lightest grenade shaped like a ball had the greatest throwing distance and accuracy. For comparison, a baseball weighs about 145 grams (compared to the 300-500 for a grenade). The circumference of a baseball is 230 mm. [The Dodger had a lot of trouble with the math for was while, but the 60 mm diameter grenade would appear to be about 180 mm circumference; this suggests grenades are denser than baseballs.] The Dodger guesses that home to second base is about 40 meters. In the Dodger's personal experience, substantial air must be put under the baseball for a non athelete to reach second base.

It would appear the reviewers should have complained about reporting distance in the abstract in this fashion. The grenadiers are not throwing for distance, they are throwing for accuracy not to overshoot the target. Presumably they would have go a lot more distance if told to really air it out. A more interesting observation is that grenadiers when throwing for accuracy fall short on the average. On the average, they missed the target by about 25 feet.

At least in movies, the Dodger remembers the grenade throwing technique as a stiff armed underhand sling, rather than overhand with follow through.

Wood Smoke vs. Diesel

Inhal Toxicol. 2005 Nov;17(12):657-70.

Responses to subchronic inhalation of low concentrations of diesel exhaust and hardwood smoke measured in rat bronchoalveolar lavage fluid.

Seagrave J, McDonald JD, Reed MD, Seilkop SK, Mauderly JL.

Lovelace Respiratory Research Institute, Albuquerque, New Mexico 87108, USA. jseagrav@LRRI.opg

Air pollution exposure is associated with adverse health effects, but the causal components and mechanisms are unclear. We compared effects of daily exposure for 6 mo to diesel exhaust (DE) or hardwood smoke (HWS) at 4 concentrations between 30 and 1000 microg/(3) of total particulate matter, or filtered air, in male and female rats. Lung lavage fluid was assayed for toxicity indicators, cytokines, and glutathione. Statistical analyses included pairwise comparisons with control and exposure-related trends, modeled using techniques that facilitated evaluation of nonlinear exposure effects. Lactate dehydrogenase increased with exposure concentration in DE-exposed females, but in other groups, low exposure concentrations caused increases while higher concentrations had less effect. Total protein in the HWS-exposed males and females followed similar patterns. Alkaline phosphatase increased in DE-exposed females, but decreased in HWS-exposed males and females. Beta-Glucuronidase decreased in HWS- and DE-exposed males, but HWS-exposed females showed decreases at low exposure concentrations and weak increases at higher exposure concentrations. Macrophage inflammatory protein-2 decreased in HWS-exposed males and females and DE-exposed females. Tumor necrosis factor-alpha levels decreased in DE-exposed females and males, but HWS-exposed males showed small increases. DE did not affect total glutathione in either gender, but HWS decreased glutathione in females, while in males, increases at low exposure concentrations but not at higher exposure levels were observed. Thus, these two combustion emissions differentially affect lung responses, with gender affecting response patterns. Furthermore, effects may be nonmonotonic functions of exposure levels, with maximal responses in environmentally or occupationally relevant exposure ranges.

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BrooklynDodger Comments: The Dodger lacks full text access to Inhalation Toxicology. So, the Dodger can't opine on no effect levels. The conclusion suggests it's in the lower end of the range, with some saturation at the higher end.

There's some interest in whether wood smoke or DPM is more toxic, we'd like to see the generation techniques. Wood contains a lot of oxygen already, as well as substantial mineral content, as well as organic components which can be distilled by heat. Wood smoke particles would likely carry some caustics. Then there's particle size, etc.

Vapor Phase Mold Emission

Environmental Health Perspectives Volume 113, Number 12, December 2005

Acute Effects of a Fungal Volatile Compound

Robert Wålinder,¹ Lena Ernstgård,² Gunnar Johanson,² Dan Norbäck,¹ Per Venge,³ and Gunilla Wieslander¹

¹Department of Medical Sciences/Occupational and Environmental Medicine, University Hospital, Uppsala, Sweden; ²Division of Work Environment Toxicology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden; ³Department of Medical Sciences/Clinical Chemistry and Asthma Research Center, University Hospital, Uppsala, Sweden

Abstract
Objective: 3-Methylfuran (3-MF) is a common fungal volatile product with active biologic properties, and previous studies have indicated a contribution to airway disease. The aim of the present study was to assess the acute health effects of this compound in humans.
Design: Acute effects were assessed via chamber exposure to (1 mg/m³) 3-MF.
Participants and measurements: Twenty-nine volunteers provided symptom reports, ocular electromyograms, measurement of eye tear film break-up time,vital staining of the eye, nasal lavage, acoustic rhinometry, transfer tests, and dynamic spirometry.
Results: No subjective ratings were significantly increased during exposure. Blinking frequency and the lavage biomarkers myeloperoxidase and lysozyme were significantly increased, and forced vital capacity was significantly decreased during exposure to 3-MF compared with air control.
Conclusions and relevance to clinical practice: Acute effects in the eyes, nose, and airways were detected and might be the result of the biologically active properties of 3-MF. Thus, 3-MF may contribute to building-related illness.
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BrooklynDodger comments: Important here are effects of a vapor phase effluent of mold. To protect against this you would need an organic vapor as well as a particulate respirator.

The report documents effects of a one or two hour exposure at about 1 mg/m3, measured in a group of 30 against whatever the background rate of variation in the biomarkers and lung function. What would be the reference level?

[The Dodger was lazy in draft. For those not afflicted with IH, the conversion from mg/m3 to ppm is MW/24.45 at room temperature. 3-MF would be C5H9O, or MW 85. So 1 mg/m3 is about 0.3 ppm]. Based on 10 fold extrapolation for acute to chronic, and another 10 fold for population variability, and another 10 for not having achieved a NOAEL, and no extrapolation for animal to human, we get a reference level of 0.003 ppm.

To the Dodger's surprise, this compound would appear unreactive and of no particular concern based on structure. So would be diacetyl, found in butter flavorings.

At a minimum, this demands that respiratory protection for mold remediation include organic vapor protection as well as particles.

Standing And Walking as Risks For Lower Extremity Disorders

Occupational and Environmental Medicine 2005;62:847-850; doi:10.1136/oem.2005.020537

Prolonged standing at work and hospitalisation due to varicose veins: a 12 year prospective study of the Danish population

F Tüchsen¹, H Hannerz¹, H Burr¹ and N Krause²

¹ Department of Surveillance and Epidemiology, National Institute of Occupational Health, Copenhagen, Denmark
² Department of Medicine, Division of Occupational and Environmental Medicine, University of California at San Francisco, USA

Department of Surveillance and Epidemiology, National Institute of Occupational Health, Lersø Parkallé 105, DK-2100 Copenhagen Ø, Denmark; ft@ami.dk

Background: Recent studies suggest that prolonged standing at work is associated with the development of diseases of varicose veins (VV).

Aims: To assess the risk of hospitalisation due to VV in the lower extremities prospectively in workers standing or walking at least 75% of their time at work.

Methods: A representative random sample of 9653 working age adults was drawn from the Central Population Register of Denmark in 1991. Of these, 8664 accepted to be interviewed by telephone (response rate 90%). Respondents (2939 men and 2708 women) were 20–59 years old and employed in 1990. Risk ratios for VV were estimated by log-linear Poisson regression models separately for men and women with adjustment for smoking status, body mass index (BMI), heavy lifting, and, for females only, number of children at baseline.

Results: During 12 years of follow up, 40 hospitalisations due to VV were observed among the men and 71 among the women. For employees with jobs that require prolonged standing or walking compared to all other employees, the relative risk was 1.75 (95% CI 0.92 to 3.34) for men and 1.82 (95% CI 1.12 to 2.95) for women. The pooled estimate of the relative risk was 1.78 (95% CI 1.19 to 2.68). The aetiological fraction of prolonged standing or walking at work was estimated as 22.5% for men and 22.6% for women.

Conclusions: This prospective study confirms that prolonged standing at work constitutes an excess risk of hospital treatment due to varicose veins and accounts for more than one fifth of all cases of working age.

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BrooklynDodger Comments: Leg and foot problems are almost never conceded by management to be work related. Hospitalization for varicose veins was about 0.1 % per year among men and twice that among women. For 30 years, thats 3% among men and 6% among women. Since everyone spends time on their feet, prolonged standing at work adds to a population background.

Welding Effects Among Naive Subjects

Post first, comment second. What do you think of the magnifying glass guy?

<<<<<<<<<<<<<<<< Is metal fume fever a determinant of welding relatedrespiratory symptoms and/or increased bronchial responsiveness? A longitudinal study
M El-Zein, C Infante-Rivard, J-L Malo, D Gautrin
. . . . . . . . . . . . . . . . . . . . . . .
Occup Environ Med 2005;62:688–694. doi: 10.1136/oem.2004.018796

Background: The current prospective study investigated the hypothesis of metal fume fever (MFF) being a predictor for the development of respiratory symptoms and functional abnormalities.
Methods: The study consisted of a pre-exposure and two follow up assessments of 286 welding
apprentices during an average period of 15 months. A respiratory and a systemic symptom questionnaire, skin prick tests to common allergens and metal salts, spirometry, and methacholine challenge tests were administered.
Results: Developing at least one positive skin prick test to a metallic salt solution was found in 11.8% of apprentices. Possible MFF (at least one of fever, feelings of flu, general malaise, chills, dry cough, metallic taste, or shortness of breath) was reported by 39.2% of apprentices. The presence of at least one welding related respiratory symptom (cough, wheezing, or chest tightness) suggestive of welding related asthma was reported by 13.8%. MFF was significantly associated with these respiratory symptoms (OR = 4.92, 95% CI 2.10 to 11.52), after adjusting for age, atopy, smoking, physician diagnosed asthma, and symptoms of non-welding related asthma. Apprentices with possible MFF, and no welding related respiratory symptoms suggestive of welding related asthma at the first follow up, had an increased risk of developing the latter symptoms by the second follow up visit (OR = 7.4, 95% CI 1.97 to 27.45) compared with those not having MFF. MFF was not significantly associated with an increase in bronchial responsiveness.
Conclusion: MFF could be a predictor for the development of respiratory symptoms but not for functional abnormalities in welders.

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BrooklynDodger Comments: An inception cohort shows clearly the effects of routine welding exposures.

These are students in 4 vocational training centers in Montreal, observed for up to 18 months. The details of their exposure regimen are found in the full paper, but it's about 2 months of welding work, according to the investigators.

No exposure data was provided by the paper.

Metal fume fever victims outnumbered those with asthma symptoms 3 to 1. MFF predicted symptoms.

This is a very short exposure. Presumably the apprentices with more severe symptoms, either MFF or asthma, will drop out of the profession, so the full risk of exposure would not be seen in a more experienced population.

Asbestos x-ray findings increase with latency

Am J Ind Med. 1994 May;25(5):635-48.

The National Sheet Metal Worker Asbestos Disease Screening Program: radiologic findings. National Sheet Metal Examination Group.

Welch LS, Michaels D, Zoloth SR.

George Washington School of Medicine, Washington, D.C.

This report presents data gathered from a series of asbestos disease screening examinations of 9,605 United States sheet metal workers who were first employed in the trade at least 20 years before the examination. The overall prevalence of asbestos-related radiographic changes was 31.1%: 18.8% had pleural abnormalities alone, 6.6% had parenchymal abnormalities (International Labour Office (ILO) score of 1/0 or higher) alone, and 5.7% had both. Among those with 40 years or more since entering the trade, 41.5% had radiographic signs of asbestos-related disease, 24.2% pleural alone, 7.7% parenchymal alone, and 9.6% both pleural and parenchymal abnormalities. After controlling for several surrogates for asbestos exposure level, cigarette smoking was found to increase risk of parenchymal, and more modestly, pleural abnormalities. Each pack-year was associated with a 1% increased prevalence odds ratios for parenchymal abnormalities (ILO category 1 compared to category 0), and 0.4% increased prevalence odds ratios for pleural abnormalities. A history of shipyard employment also produced significantly increased prevalence odds ratios for each radiographic category. More that 90% of chest radiographs were classified by A or B readers; after adjustment for other risk factors, A readers were more likely to report parenchymal abnormalities of category 1, but not more likely to report category 2 or pleural abnormalities, than B readers.

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BrooklynDodger comments: This abstract came up as the Dodger was thinking about a reheating of asbestos compensation legislation.

A notable feature of union based asbestos screening programs was involvement of quality occupational health scientists who could put the results into the peer reviewed literature. These results provide real useful data for public health purposes.

A key dispute is whether a lung cancer victim with asbestos exposure gets compensated in the absence of x-ray evidence of asbestos effect. This paper sheds important light on the importance of latency in observing x-ray evidence of asbestos effect. The Dodger doesn't have access to the full text of the paper, so these comments are based on the abstract. To get into the study, you needed 20 years of latency, years since hired. Overall, there were 31% with x-ray abnormalities, but with 40 years latency there were 41%, suggesting a near doubling in rate from 20 to 40 years. The appearance of x-ray findings appears a combination of ripening of scarring from past exposure with increasing scarring from more exposure with longer duration.

Remember the "Blue Collar Blues?"

Remember, the Dodger is now posting the edited or highlighted abstract first, and the comments below. Occup Environ Med. 2004 Aug;61(8):668-74. Ergonomic stressors and upper extremity musculoskeletal disorders in automobile manufacturing: a one year follow up study. Punnett L, Gold J, Katz JN, Gore R, Wegman DH. Department of Work Environment, University of Massachusetts Lowell, One University Avenue, Lowell, MA 01854, USA. Laura_Punnett@uml.edu AIMS: To estimate the one year cumulative incidence and persistence of upper extremity (UE) soft tissue disorders, in a fixed cohort of automotive manufacturing workers, and to quantify their associations with ergonomic exposures. METHODS: At baseline and at follow up, cases of UE musculoskeletal disorders were determined by interviewer administered questionnaire and standardised physical examination of the upper extremities. The interview obtained new data on psychosocial strain and updated the medical and work histories. An index of exposure to ergonomic stressors, obtained at baseline interview, was the primary independent variable. Cumulative incidence and persistence of UE disorders (defined both by symptoms and by physical examination plus symptoms) were analysed in relation to baseline ergonomic exposures, adjusting for other covariates. The incidence of new disorders was modelled using multivariate proportional hazards regression among workers who were not cases in the first year and the prevalence on both occasions was modelled by repeated measures analysis. RESULTS: A total of 820 workers (69% of eligible cohort members) was examined. Follow up varied slightly by department group but not by baseline exposure level or other characteristics. Among the non-cases at baseline, the cumulative incidence of UE disorders was 14% by symptoms and 12% by symptoms plus examination findings. These rates increased with index of physical exposures primarily among subjects who had the same jobs at follow up as at baseline. Increased exposure during follow up increased risk of incidence. The persistence of UE disorders from baseline to follow up examination was nearly 60% and somewhat associated with baseline exposure score. CONCLUSIONS: These longitudinal results confirm the previous cross sectional associations of UE musculoskeletal disorders with exposure to combined ergonomic stressors. The exposure-response relation was similar for incident cases defined by symptoms alone and those confirmed by physical examination. >>>>>>>>>>>>>>>>>>>>>>>>>>>>>> BrooklynDodger Comments: Remember the "blue collar blues," when the hazard of working the assembly line was boredom? This paper examines workers in stamping and engine manufacture, rather than the vehicle assembly line. Rates of injury, and MSD, are lower in these parts manufacture operations than vehicle assembly overall, although the difference narrows when restricting attention only to machine operators and assemblers in both operations [rates are less, and penetration is higher for skilled trades in parts manufacture vs. assembly.] The investigators neglected to include the fraction of workers with MSD at baseline, which was about 35%. This was somewhat lower than observed in other investigations [Bernard et al, not published]. So, given 60% persistence, that's about 15% of the population resolving their MSD which about 13% suffered a new one, for a steady state. This prevelence is upper extremity only, and doesn't include back, which is common, and foot-ankle-leg, which is probably also common but there's no data. Anyway, a good chunk of the unhappiness called the "blue collar blues" is likely the sequel to working in pain for long periods if not always.

X-Ray Doesn't Predict Increased Risk of Pleural Mesothelioma Beyond Exposure

Occup Environ Med. 2005 Oct;62(10):665-9.

The additional risk of malignant mesothelioma in former workers and residents of Wittenoom with benign pleural disease or asbestosis.

Reid A, de Klerk N, Ambrosini G, Olsen N, Pang SC, Musk AW.

School of Population Health, University of Western Australia, Australia.

AIMS: To examine the hypothesis that people with benign pleural disease or asbestosis have an increased risk of malignant mesothelioma beyond that attributable to their degree of asbestos exposure. METHODS: Former workers and residents of the crocidolite mining and milling town of Wittenoom are participating in a cancer prevention programme (n = 1988). The first plain chest radiograph taken at the time of recruitment into the cancer prevention programme was read for evidence of benign pleural disease and asbestosis, using the UICC classification. Crocidolite exposure of former workers was derived from employment records and records of dust measurements performed during the operation of the asbestos mine and mill between 1943 and 1966. Based on fibre counts, exposure for former residents was determined using duration of residence and period of residence (before and after a new mill was commissioned in 1957) and interpolation from periodic hygienic measures undertaken from personal monitors between 1966 and 1992. Cox proportional hazards modelling was used to relate benign pleural disease, asbestosis, asbestos exposure, and mesothelioma. RESULTS: Between 1990 and 2002, there were 76 cases of mesothelioma (56 of the pleura and 20 of the peritoneum). Cases had more radiographic evidence of (all) benign pleural disease, pleural thickening, blunt/obliterated costophrenic angle, and asbestosis than non-cases. Adjusting for time since first exposure (log years), cumulative exposure (log f/ml-years), and age at the start of the programme, pleural thickening (OR = 3.1, 95% CI 1.2 to 7.6) and asbestosis (OR = 3.3, 95% CI 1.3 to 8.6) were associated with an increased risk of peritoneal mesothelioma. There was no increased risk for pleural mesothelioma. CONCLUSION: The presence of benign pleural disease, in particular pleural thickening, and asbestosis appears to increase the risk of mesothelioma of the peritoneum, but not of the pleura beyond that attributable to indices of asbestos exposure in this cohort of subjects exposed to crocidolite.

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BrooklynDodger Comments: This paper reflects back to the asbestos compensation legislation, indirectly. Relationship to non-malignant asbestos findings on x-ray [nothing is benign about asbestos] and malignancy is key to a formula for who gets what.

Higher population rates for lung cancer obscure the low exposure exposure response relationship for lung cancer.

Residential cases confirm the low exposure risk of asbestos. It's not surprising that increased exposure [level duration latency] increased risk of x-ray findings. When adjusted for asbestos exposure, x-ray findings did not predict pleural mesothelioma risk, suggesting the two disease processes are uncoupled. Not so for peritoneal meso.

A recent paper suggests peritoneal meso treatment results are optimistic, in contrast to pleural.

Injury Control at NSC

For some reason, the National Safety council chose to list the following as the

Fact of the week
9 out of 10
Number of worker fatalities that occur off the job.

Source: National Safety Council, "Injury Facts" 2004

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BrooklynDodger has no problem with NSC arguing that more should be done to control injuries in the community, outside work. The Dodger, however, can help thinking the factoid above impacts management in the direction of reducing workplace prevention. The denominator supporting the 9 0f 10 estimate is likely the working age fraction of the 80,000 unintentional injury deaths suffered each year.

The Dodger will return to whether seat belts and drunk driving are the best approach to preventing the 44,000 traffic fatalities.

http://www.nsc.org/library/report_injury_usa.htm

National Safety Council Recommendations to Reduce Injuries

• Strengthen safety belt laws nationwide to reduce traffic fatalities.
• Encourage companies and organizations to enact strict buckle-up policies for employees.
• Install handrails, grab bars and night-lights in homes to reduce the risk of falls.
• Keep all medicine/cleaners out of sight in cabinets with child-proof latches to stop poisonings.
• Encourage every adult American to learn first aid/CPR.

Occupational Injury and Disability Discrimination

BrooklynDodger brings this to the occupational blog because it's an occupational situation. Larry Brown's osteoarthritis of the hip was almost certainly of occupational origin. [The Dodger did look it up.] The condition might have been caused by playing or running up and down the court coaching for any number of employers, but it was undoubtably aggravated during Brown's previous year for the Pistons. The employee was under no obligation to schedule the hip surgery in relation to the employers needs, nevertheless, Larry did so, and returned to work on time. The bladder problem is a known consequence of the hip surgery. [The Dodger did look it up.] It appears Larry couldn't pee, not that he had to leave the court in the 4th quarter. Nevertheless, it falls in the caused or aggravated catergory. The history reads like a workers compensation or ADA retaliation case. PS: What's up with the Mayo Clinic? BrooklynDodger recalls that the 2,000 year old man also went to the Mayo Clinic >>>>>>>>>>>>>>>>>>>>>>>>>> Motown reunion

Larry's health an issue as he returns to Detroit

BY FRANK ISOLA DAILY NEWS SPORTS WRITER

Larry Brown brings Knicks, and questions about his health, with him to Detroit. The uncertainty regarding Larry Brown's health, a major factor in the Detroit Pistons' decision to sever ties with the Hall of Fame coach last July, could become a troubling issue for the Knicks. On eve of his emotional return to Detroit, Brown revealed that he'll need additional surgery to correct a bladder condition and that he has decided to postpone the procedure until after the season. Brown added that he's "pretty confident" he'll be healthy enough to coach all 82 regular season games but he wouldn't guarantee it. "I've been in the hospital twice in the last three weeks and I think I feel like I got to wait until after the season to get some things taken care of," Brown said during a conference call. "If I did something now it would keep me out. But if I did it after the season I would have ample time, I think, to get back and get ready to go again." Brown, 65, has attended every Knicks practice and game since signing a five-year, $50 million contract on July 27. The two hospital visits he refereed to did not include an overnight stay. Brown underwent hip surgery last November and then in March he needed surgery for a bladder problem. He missed a total of 17 games last season. The questions over Brown's health and his availability worried the Pistons, who were also upset that Brown was flirting with Cleveland about becoming their top basketball executive while the Pistons were in the midst of trying to win back-to-back NBA championships. William Davidson, the team's reclusive owner, even came out publicly to say that Brown wasn't "a good person." "It troubles me that he thought I was a bad guy," Brown said. "I did everything I possibly could to coach the team to the best of my ability. .. Although Brown continues to claim he was fired, he received $7 million of the $18 million he was owed which smells more like a negotiated buy-out... But Brown also reiterated that he was forced to come back too soon from the hip surgery and hinted that not everyone in the organization believed he had a serious medical condition. "I was a sked to come back after my first surgery and I did," he said. "I didn't know I was going to have a problem physically. I think that hurt. When I had the hip problem and the problems after that it affected our team. I don't think that's what they were willing to risk this season. I understand that. I think Mr. Davidson made that pretty clear to me. "I thought if I would be back coaching it would be in Detroit or I wouldn't be coaching because of my health. That's why I wanted as soon as I could to go to the Mayo Clinic and get checked. I thought it was important to let them known quickly because I think it was an issue. I never deviated from saying that if I would coach again I was hopeful that I would be healthy enough to go back to Detroit. But again, they made a decision that they thought was in the best interest of their team. I don't have a problem with that.... Originally published on December 1, 2005

Asbestos and Colon Cancer

BrooklynDodger herewith adopts a new format for posting journal abstracts. The abstract, highlighted or excerpted will lead. The Dodger's commentary will follow. >>>>>>>>>>>>>>>>>>>>>>>>>>> Am J Epidemiol. 2005 Nov 1;162(9):868-78. Epub 2005 Sep 21.

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.

Cancer Center, Yale University School of Medicine, New Haven, CT, USA.

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.

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BrooklynDodger's Comments: An association between asbestos and colon or other digestive cancers is still in play. Asbestos fibers were found in Lake Superior waters, polluted by taconite tailings from Reserve Mining. Did they pose a cancer risk? Did uncontroverted evidence for lung cancer by inhalation in people also support a cancer risk at any site from ingestion of fibers? Was colon cancer a consequence of asbestos at work, either by direct ingestion or recycled fibers swallowed from the respiratory tract?

There's an NAS committee at work on this subject today.

An NAS bioassay of ingested asbestos in rats and mice did not observe an association. The Dodger will go back into ancient history on that, but bottom line is that rats are very resistent to asbestos fibers by inhalation, and mice are totally resistence. These rodents are not models for colon cancer [meaning, they don't get it much, and not after treatment by carcinogens.]

The CARET trial, in the author's words, "suggests" an association. The limitation to smokers arises because only smokers were allowed in the CARET trial.

The Dodger will return to the bioassay and the present controversy soon.