Hierarchy of Controls on the Road [corrected]

Brooklyn Dodger argues that evidence based interventions based on the hierarchy of controls are needed to reduce traffic injuries. The most dangerous conditions for fatalities are rural, two lane roads. Probably speeding on curved roads going down hill at night in the rain would be the highest of the high risk. Strict enforcement of speed limits in rural areas would be as popular as gun control. There will still be curves in the road, night will fall and the weather will be bad, and freeways won’t go everywhere. What to do?

This study demonstrates a low cost control, rumble strips down the center line. Why didn’t the Dodger think of that? Why doesn’t someone install them? Where are the National Safety Council and Department of Transportation?

Paraphrased abstract:

Vehicles crossing the centerline and either sideswiping or striking the front ends of opposing vehicles account for about 20% all fatal crashes on rural two-lane roads and result in about 4500 fatalities annually in the US. Data were analyzed for approximately 210 miles roads in seven states before and after installation of centerline rumble strips. Significant reductions for all injury crashes combined, 14%, as well as for frontal and opposing-direction sideswipe injury crashes, 25%, were observed.

VVVVVVVVVVVVVVVVVVVVVVVVVV

Accident Analysis & Prevention Volume 36, Issue 6 , November 2004, Pages 1073-1079

Crash reduction following installation of centerline rumble strips on rural two-lane roads

Bhagwant N. Persaud , , a, Richard A. Rettingb and Craig A. Lyona a Department of Civil Engineering, Ryerson University, 350 Victoria Street, Toronto, Canada M5B 2K3b Insurance Institute for Highway Safety, 1005 North Glebe Road, Arlington, VA 22201, USA Received 2 December 2003; Revised 12 March 2004; accepted 17 March 2004. Available online 20 June 2004.

Ambient Particles Instilled in People at Very Low Doses Cause Airway Inflammation

BrooklynDodger repeatedly points to the burst of research findings showing adverse health effects of ambient air particle pollution at levels of exposure permitted by EPA limits. The Dodger has argued that mass of small particles or particle count – both available in real time by direct reading instruments – is the best measure, certainly the most convenient. Particles with no special toxicity – carbon black, amorphous silica – appear equally potent in animal systems to diesel particulate matter, and much more potent than cigarette smoke. Expensive chemical analysis only gets in the way, and opens the field to special pleading and Houdini risk assessments.

Nevertheless, the Dodger concedes that chemical composition could be a modifier or intensifier of the effect. Metal particles in the air are expected to be oxides generate from combustion products; PM 2.5 particles are expected to be agglomerations of smaller particles immediately generated by combustion. Cadmium oxide, chromium (VI) oxide are plausibly more potent carcinogens [now the Dodger has to look this up.] Iron oxide – probably the most weighty of these metal compounds – can be thought of as delivering oxidative power in concentrated form to the cell membranes of the respiratory system.

The Dodger reminds readers that these exposure levels are much less than typically encountered in the workplace.

The paper summarized below is premised on a connection between tissue damage to the respiratory system and asthma, which may be incorrect. However, it demonstrates the potency of particles concentrated from ambient air, and suggests greater potency for metal rich particles:

Investigators compared effects of particles from a German smelter area known to have increased asthma in children to a non-industrialized area…100 µg of PM2.5 suspensions, collected simultaneously in the two areas, were instilled through a bronchoscope into healthy volunteers. [This would be equivalent to 10 µg/M3 averaged over a work shift.] PM2.5 from both areas increased the number of white cells in the bronchoalveolar lavage performed 24 hours later. PM2.5 from the smelter area, but not the clean area, induced a significant influx of monocytes. Oxidant radical generation of bronchoalveolar lavage cells and cytokine concentration (interleukin-6 and tumor necrosis factor-alpha) in bronchoalveolar lavage fluid was significantly increased after instillation of Hettstedt PM2.5.

The invesgtigators concluded that environmentally relevant concentrations of PM2.5 from the smelter area induced distinct airway inflammation in healthy subjects with a selective influx of monocytes and increased generation of oxidant radicals. The higher concentration of transition metals in PM2.5 from smelter area might be responsible for this increased inflammation.

VVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVV

Am J Respir Crit Care Med. 2004 Oct 15;170(8):898-903.

Metal-rich Ambient Particles (Particulate Matter2.5) Cause Airway Inflammation in Healthy Subjects

Frank Schaumann, Paul J. A. Borm, Andreas Herbrich, Johannes Knoch, Mike Pitz, Roel P. F. Schins, Birgit Luettig, Jens M. Hohlfeld, Joachim Heinrich and Norbert Krug

Fraunhofer Institute of Toxicology and Experimental Medicine, Hannover; Institut für Umweltmedizinische Forschung, Duesseldorf; and GSF-National Research Center for Environment and Health, Institute of Epidemiology, Neuherberg, Germany
Correspondence and requests for reprints should be addressed to Norbert Krug, M.D., Fraunhofer Institute of Toxicology and Experimental Medicine, Nikolai-Fuchs-Str. 1, Hannover 30625, Germany. E-mail: krug@item.fraunhofer.de

Sleep Deprivation and Time Awake Decreases Driving Performance - A key to off-the-job injury prevention which applies on the Job as well

BrooklynDodger believes that extended work hours cause traffic accidents. A worksite-based off-the-job injury program must address this. Time since waking is probably the best measure of increased risk. Prior sleep deprivation increases risk when added to time since waking.

These findings are more important than driving - they probe the effect of work hours on all types of errors, including both those which cause injury and those which cause production and quality problems.

In this study, the sleep restricted drivers arrived in the lab at 9 pm, had 2 hours sleep, and started driving 8 hours after waking, continuing to drive until 18 hours. The unrestricted drivers started driving 1 ½ hours after waking and continued to drive until 11 ½ hours after waking. From the first cycle, the sleep restricted drivers were driving poorly. Rested drivers also showed decreased performance later in the driving cycle.

The investigators concluded “Our findings show that duration of driving is not the main factor to explain driving impairment and that time awake and previous sleep duration have a much bigger impact. Professional regulations and work schedules should integrate sleep schedules before and during the work period as an essential dimension for safe driving.”


Decline in Driving Performance over a 10 hour period

VVVVVVVVVVVVVVVVVVVVVVVVVVVVVVV
Edited abstract and summary:

Healthy young males drove 625 miles with a co-pilot over 10 h during five 105 min sessions on an open [French] highway. In the sleep restriction condition, subjects were allowed to sleep only from 23:00 to 01:00. All drivers started driving at 9 am and drove 5 sessions with breaks ending at 7 pm. Subjects were instructed to maintain a constant speed (130 kph or 80 mph) and not to cross the painted lines separating the lanes except to pass a slower vehicle. Self-rated fatigue and sleepiness were recorded before each session, number of inappropriate line crossings from video recordings and simple reaction time (RT) were measured.

In the rested condition, co-pilots never interfered with driving. In the sleep-restricted condition, co-pilots interfered 61 times with the driving of subjects and several had to stop because of fatigue. No subjects had to stop driving during the rested condition. Line crossings increased during the day for both rested and restricted subjects.

Line crossings increased 8-fold with sleep restriction (535 crossings in the sleep-restricted condition versus 66 after non-restricted sleep). Crossings increased with increasing sleepiness score during the next driving session in the sleep-restricted. Rested subjects drove 1000 km with four shorts breaks with a minor performance decrease [Minor is in the eye of the other drivers, this was still an effect]. Sleep restriction induced important performance degradation even though time awake (8 h) and session driving times (105 min) were relatively short. Performance degradation was associated with sleepiness and not fatigue. Sleepiness combined with fatigue significantly slowed reaction time.

VVVVVVVVVVVVVVVVVVVVVVV

Accident Analysis & Prevention Volume 37, Issue 3 , May 2005, Pages 473-478

Fatigue, sleep restriction and driving performance

Pierre Philipa, , , Patricia Sagaspeb, Nicholas Moorec, Jacques Taillarda, André Charlesb, Christian Guilleminaultd and Bernard Bioulaca aClinique du Sommeil, CHU Pellegrin, Place Amelie Raba Leon, 33076 Bordeaux Cedex, FrancebLaboratoire de Psychologie, EA 3662, Université Bordeaux II, 33076 Bordeaux Cedex, FrancecDépartement de Pharmacologie, Université Bordeaux II, 33076 Bordeaux Cedex, FrancedSleep Research Center, Stanford Medical School, Stanford, CA, USA

Self Blogilation

BrooklynDodger confesses to self-googling. The blog itself appears invisible, but references are found on other blogs. Not knowing how to put in reciprocal links, the Dodger posts the following site which recognized this site.

http://effectmeasure.blogspot.com/2005/03/blog-rollin-friday-brooklyndodger.html

Effect Measure [also by anonymized Public Health types]

Off the Job Injuries

BrooklynDodger returns to off-the-job injuries.

Occupational health staff are being pressured to generate off-the-job injury programs. To avoid pure blame the victim approaches, and to consider the hierarchy of controls, it would be valuable to know something about these off-the-job injuries.

The Dodger notes that many “off-the-job” injuries are actually on-the-job injuries carried home and treated away from work. These on-job caused injuries may be off-job treated to hide them from punitive employer programs, or just because it’s more convenient and with more patient control to go outside.

The Consumer Product Safety Commission (CPSC) National Electronic Injury Surveillance System (NEISS) collects data on all types and external causes of nonfatal injuries and poisonings treated in U.S. hospital emergency departments (EDs). Approximately 31,000,000 persons were treated for nonfatal injuries in EDs in 2000. Most of the injuries were unintentional but an estimated 1,973,000 (6.4%) were violence-related.

[ICD-9-CM external cause-of-injury codes were not assigned. Safety folks should review these causes for utility in the occupational setting.]

During 2000, an estimated rate of 11,188 per 100,000 population were treated, over 10%. The nonfatal injury rate was approximately 40% higher for males than for females. Falls were the leading cause of unintentional nonfatal injuries, 24.4%. [The Dodger has heard somewhere that the most dangerous consumer product is stairs.] About 17% were transport related. Overexertion caused 10.5% of cases. So the top three are about 50%.These cause codes are somewhat informative about prevention of injury. Other causes, such as "struck by," at 17.4%, were not informative.

CPSC maintains an open website somewhere for generating reports at

http://www.cpsc.gov/library/neiss.html. These queries could generate data on working age people, to inform off-the-job safety programs delivered on job. BrooklynDodger has not been very successful using this site.


VVVVVVVVVVVVVVVVVVVVVV

http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5017a4.htm

National Estimates of Nonfatal Injuries Treated in Hospital Emergency Departments --- United States, 2000

Reported by: Office of Statistics and Programming, National Center for Injury Prevention and Control, CDC.

Don’t Stop Thinking About Tomorrow … But Think Less about Yesterday [an essay with no references]

Back in the day – mid ‘70’s – it seemed like there were maybe 4 lung carcinogens: cigarette smoke, asbestos, radon, and coke oven emissions. Notably, all of these made the list based on studies in people, with little or no laboratory toxicology to back it up.

Based on the distribution of exposures to this gang of only 4, Peto and Doll issued a canonical statement that only 2% of cancers were due to “pollution” or industrial chemicals. http://www.cato.org/testimony/ct-mg030697.html Additionally, the only hints of airborne contaminants causing heart disease were carbon monoxide, or fibrotic exposures stressing the heart.

The Peto-Doll estimate was faulty even with what was known then. Cigarette smoke was then known to potentiate other lung carcinogens, asbestos and radon, yet all the cancers were attributed to the demon leaf. Hold this thought for later.

BrooklynDodger remembers when many devoted their research efforts to explaining why asbestos caused fibrosis and lung cancer, while silica caused only fibrosis and not lung cancer.

Many in the IH community are still stuck in yesterday. Here’s where we are today. These comments track a parallelogram whose sides are: health effects in animals from exposures known to be carcinogenic in people; and, health effects in people of exposures known to be carcinogenic in animals.
The first idol to fall was silica. Silica was tested in animals, first as a non-cancer but fibrogenic control for oil shale dust, and then as part of an assay of Mt. St. Helen’s dust. All the carcinogenesis of oil shale was due to Silica. Silica was carcinogenic in the rat. This provided biological plausibility to the more than 50 studies showing silica to cause excess cancer in workers. Finally, a study in Vermont granite workers put silica over the top as a known human carcinogen.

Diesel particulate matter should have altered another paradigm. DPM was initially a concern as a tobacco or coke oven emissions surrogate – carbon-containing particles with heavy organic carcinogens adsorbed onto the surface. Extracts from DPM particles were mutagenic in bacterial bioassays. Simultaneously, EPA and industry money started laboratory bioassays and mortality studies in workers exposed in trucking and on the railroads. DPM turned out to about 100 times as potent a carcinogen in the rat as cigarette smoke [which is barely carcinogenic at all in the lab.] Meanwhile, about two dozen studies in railroad, trucking and some miners found excess lung cancer, including studies taking smoking into account. [Smoking is never the cause of increased lung cancer in an occupational cohort.] Then a bioassay of carbon black – diesel with the gooey carcinogens washed away – was positive as well.

Non asbestos [baby grade] talc proved carcinogenic in a laboratory bioassay in the rat.

A series of community studies found increase mortality from respiratory illness [no biological surprise] and cardiac diagnoses [a big surprise] with increases in particulate pollution. This sparked a wave of laboratory studies showing that fine particles – 0.3 micron – penetrated the lung into systemic circulation. Which means that remote site tumors from cigarette smoke and coke oven emissions may be a direct particle effect rather than a surface carcinogen desorbed and absorbed effect.

Radon’s human carcinogenic effect was observed in miners. At the time these studies were done, silica was not yet a carcinogen, so silica exposure was not taken into account. Almost certainly, the cancers in the miners were a joint effect of radon [daughters] and silica, so radon potency is overstated, and the fraction of cancers due to radon is also overstated.

Environmental tobacco smoke was declared a known human carcinogen, based on household studies comparing non smoking spouses of smokers to non smoking spouses on non smokers.

How do these dots connect?

Everyone, everywhere, inhales mineral and carbon particles constantly, even without specific occupational exposures. These previously inert particles are much more potent than tobacco smoke, but for smokers there’s a lot more tobacco smoke. For ETS exposed people, potency differences mean that ETS is likely the tail wagging the particle dog. The same goes for radon, where ignoring particle toxicity [in the mines] leads to recommendations that people move out or tear down their houses.

For us old dog industrial hygienists, the earth needs to move from 5000 micrograms of “nuisance” dust being nearly ok, to worrying about 50 micrograms of particles NOS as a cancer risk.

Disability by Cause - Hints at Prevention

Most work related disability presents as non-work related, or at least is uncounted as caused by work. Cause specific data suggests preventive measures. The National Health Interview Survey Disability Supplement permitted examining factors associated with employment among Americans with disabilities. Persons with disabilities related to cardiovascular disease (OR, 0.23), musculoskeletal disease (OR, 0.37), and respiratory disease (OR, 0.23) were less likely to work than other Americans with disabilities. Persons with self-reported alcohol abuse (OR, 1.30) were more likely to work, and persons with self-reported drug abuse (OR, 0.93) were not less likely to work, than others in our study population of Americans with disabilities.

So, musculoskeletal jumps out once again as a major source of problem. And, alcohol and drug abuse get a clean bill.

J Occup Environ Med. 2002 Apr;44(4):358-64.

Workforce participation by persons with disabilities: the National Health Interview Survey Disability Supplement, 1994 to 1995.

Zwerling C, Whitten PS, Sprince NL, Davis CS, Wallace RB, Blanck PD, Heeringa SG.University of Iowa, College of Public Health, 100 Oakdale Campus, #126 IREH, Iowa City, IA 52242-5000, USA.

CZwerling@mail.public-health.uiowa.edu

Don't Fall Down

BrooklynDodger returns to off-the-job injuries.

Occupational health people are pressured to generate an off-the-job injury program. To avoid pure blame-the-victim approaches, and to consider the hierarchy of controls, it would be valuable to know something about these off-the-job injuries. The Dodger notes that many “off-the-job” injuries are actually on-the-job injuries carried home and treated away from work. These on-job caused injuries may be off-job treated to hide them from punitive employer programs, or just because it’s more convenient and with more patient control to go outside.

The Consumer Product Safety Commission (CPSC) National Electronic Injury Surveillance System (NEISS) collects data on all types and external causes of nonfatal injuries and poisonings treated in U.S. hospital emergency departments (EDs). Approximately 31,000,000 persons were treated for nonfatal injuries in EDs in 2000. Most of the injuries were unintentional but an estimated 1,973,000 (6.4%) were violence-related.

[ICD-9-CM external cause-of-injury codes were not assigned. Safety folks should review these causes for utility in the occupational setting.]

During 2000, an estimated rate of 11,188 per 100,000 population were treated, over 10%. The nonfatal injury rate was approximately 40% higher for males than for females. Falls were the leading cause of unintentional nonfatal injuries, 24.4%. About 17% were transport related. Overexertion caused 10.5% of cases. These cause codes are somewhat informative about prevention of injury. Other causes, such as struck by, at 17.4%, were not informative.

CPSC maintains an open website somewhere for generating reports at

http://www.cpsc.gov/library/neiss.html.

These queries could generate data on working age people, to inform off-the-job safety programs delivered on job. BrooklynDodger has not been very successful using this site. Others may be.

VVVVVVVVVVVVVVVVVVVVVVVVVV

http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5017a4.htm

National Estimates of Nonfatal Injuries Treated in Hospital Emergency Departments --- United States, 2000

Chemoprevention Strike Two

Recently there’s been some attention paid to the CARET study, a chemoprevention study in which heavy smokers [really heavy smokers] and asbestos exposed workers were provided Vitamin A to test whether anti-oxidants retard development of lung cancers. Instead, it was found that the treatment accelerated the development of lung cancers. The study was stopped.

Diet and cancer studies suggest various “healthy” practices, including anti oxidant intake protect against cancer. By discrediting the biological basis for Vitamin A protection, the CARET study suggests that maybe all the “healthy living protects” results are uncontrolled confounding.

The study reported here added Vitamin E. About 30,000 male Finnish smokers were followed for up to 8 years. No reduction in incidence was observed among the men who received vitamin E. A higher incidence of lung cancer among the men who received Vitamin A than among those who did not. Fewer cases of prostate cancer were diagnosed among those who received alpha-tocopherol than among those who did not. Beta carotene had little or no effect on the incidence of cancer other than lung cancer. Alpha-tocopherol had no apparent effect on total mortality. Total mortality was 8 percent higher (95 percent confidence interval, 1 to 16 percent) among the participants who received beta carotene than among those who did not, primarily because there were more deaths from lung cancer and ischemic heart disease.


VVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVV

http://content.nejm.org/cgi/content/abstract/330/15/1029?ijkey=a28c00875a55e4c8979acd9eab4515ed1a703184&keytype2=tf_ipsecsha

The Effect of Vitamin E and Beta Carotene on the Incidence of Lung Cancer and Other Cancers in Male Smokers

Beta Carotene Cancer Prevention Study Group The Alpha-Tocopherol

NEJM Volume 330:1029-1035 April 14, 1994

Job Strain and Heart Attack: Not as null as presented.

BrooklynDodger here presents a null study for the association of job strain with adverse health outcomes. The study is not as null as the abstract says. The Dodger again exhorts reviewers and editors to pay more attention to abstracts.

The Belgian study reports 87 cardiac events over 3 years in 14,377 middle aged men. [These are a lot of people, but very few events, especially distributed over 3 or 4 levels of fuzzy variables.] 17% of the workers experienced high strain. The investigators concluded job demands and decision latitude were not significantly related to the development of coronary heart disease. The investigators noted that a 38% risk excess among subjects in the high-strain category did not reach statistical significance [but neglected to include the confidence interval in the abstract. The Dodger would have to go into the full text paper to find the number of cases and the confidence interval.] The investigators noted that coronary heart disease incidence was substantially associated with the social support scale [The Dodger assumes they meant risk goes up as social support goes down. Doesn’t anyone edit these abstracts? They could have said “negatively correlated,” which would be poor diction but at least accurate] independently of other risk factors.

The Dodger feels the conclusion “No convincing evidence for an association of … job strain with the short-term incidence of coronary heart disease was found.” to be unfounded. The upper CI of the high job strain was 2.38, based on 18 cases. A 38% increased risk of heart attack, which could have been a more than doubling a risk is nothing to blow off, when the study clearly had little power. It would have been more accurate to say that the study, which may have been inadequate, provided “equivocal” or “some” evidence.

A perception of low social support was indeed associated with higher risk. The Dodger has glanced at a version of this standard job content questionnaire. There are limited objective elements in the job demands questions [for example “I have to work very fast”]. The social support questions pretty much elicit subjects’ subjective response to the environment. Well, the paper does say “perceived” job stress.

VVVVVVVVVVVVVVVVVVVVVVVVVVVVVV

Am J Epidemiol. 2005 Mar 1;161(5):434-41.

Perceived Job Stress and Incidence of Coronary Events: 3-Year Follow-up of the Belgian Job Stress Project Cohort.

De Bacquer D, Pelfrene E, Clays E, Mak R, Moreau M, de Smet P, Kornitzer M, De Backer G.Department of Public Health, Ghent University, Ghent, Belgium.

More on Vitamin A Causing Cancer

The asbestos arm of the asbestos and smoking chemoprevention study are critical to the asbestos compensation bill now before the Senate Judiciary Committee. BrooklynDodger will post on that soon. The overall study enrolled a large group of very heavy smokers as well as asbestos workers with all levels of smoking. Posted below is title information to lead you to the full abstract of that study.

The key conclusions were: "The previously reported adverse effects of beta-carotene and retinyl palmitate on lung cancer incidence and all-cause mortality in cigarette smokers and individuals with occupational exposure to asbestos persisted after drug [vitamin A] administration was stopped although they are no longer statistically significant.... the excess risks of lung cancer [in the post administration period, relative to other similarly exposed] were restricted primarily to females, and cardiovascular disease mortality primarily to females and to former smokers."

[The full text may be available from JNCI, a lot of the federal journals now have free web access.]

BrooklynDodger had previously opined that estimates of lung cancer effects of smoking should be modified to take into account the independent effect of newly identified carcinogens such as silica, diesel particulate matter, carbon black, metal oxides [as identified in welding fume] as well as synergistic effects. If carbon black is carcinogenic, then perhaps all particles are carcinogenic, including the massive particle exposure to cigarette smoke.

This study was launched based on diet studies in a general population [that is, a population without exposure assessment] which observed reduced lung cancer among those with high anti-oxident

BrooklynDodger suggests that an effect seen in females but not males may be an artifact of lower general population rates in females, and less variation in exposure in the females, rather than a real differential effect between men and women.


VVVVVVVVVVVVVVVVVVVVVVVVVVVV

J Natl Cancer Inst. 2004 Dec 1;96(23):1743-50.

The Beta-Carotene and Retinol Efficacy Trial: incidence of lung cancer
and cardiovascular disease mortality during 6-year follow-up after
stopping beta-carotene and retinol supplements.

Goodman GE, Thornquist MD, Balmes J, Cullen MR, Meyskens FL Jr, Omenn
GS, Valanis B, Williams JH Jr.
Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. North, Bldg.
M, M1-B514, Seattle, WA 98109, USA. gary.goodman@swedish.org

Hiatus

On hiatus for a week. The system to which I go won't allow posting to blogspot.

Wal-Mart Threatens Your Safety, Even if You Don't Work There

Drowsy driving is a big risk factor for collisions. Research shows that the interval from waking up is the biggest predictor of sleepiness [not a surprise, but better to have data] than how long someone has been driving. Since regulation of when someone debunks [that is, gets out of bed, a surrogate for waking up] is tough, a reasonable surrogate is time on the clock.

Nearly 5,000 people were killed in large truck crashes in 2003, and those vehicles were three times more likely to be involved in fatal crashes than passenger cars, according to the National Highway Transportation Safety Administration.

The new motor carrier regulation required drivers to stop after 14 hours on the clock, and, more important, 60 hours in the week. That rule had been struck down in federal court because it didn't take into account truck drivers' health. In October, Congress reinstated the rule for one year. It a breath taking display of corporate arrogance, an Arkansas congressman proposes to make bad even worse.


http://www.cnn.com/2005/US/03/08/trucker.rules.ap/index.html

Retailers want 16-hour trucker workday
Critics: 'Sweatshop-on-wheels amendment'

Tuesday, March 8, 2005 Posted: 7:35 PM EST (0035 GMT)

WASHINGTON (AP) -- Wal-Mart and other retailers are lobbying Congress to extend the workday for truckers to 16 hours, something labor unions and safety advocates say would make roadways more dangerous for all drivers.
Rep. John Boozman, an Arkansas Republican whose district includes Wal-Mart's headquarters in Bentonville, is sponsoring a bill that would allow a 16-hour workday as long as the trucker took an unpaid two-hour break.

Data on how bad the situation is are provided by a paper in a leading peer reviewed journal:

Data on the prevalence and hypothesized predictors of falling asleep while driving were gathered through face-to-face interviews with 593 long-distance truck drivers....... 47.1% of the survey respondents had ever fallen asleep at the wheel of a truck, and 25.4% had fallen asleep at the wheel in the past year. ...Six underlying, independent factors predicted falling asleep: greater daytime sleepiness; more arduous schedules, with more hours of work and fewer hours off-duty; older, more experienced drivers; shorter, poorer sleep on road; symptoms of sleep disorder; and greater tendency to night-time drowsy driving. ...Drivers who had fallen asleep at the wheel had higher scores on the arduous work schedule factor; these were drivers who typically drove longer than the 10 consecutive h allowedby regulation, took fewer than the 8 h off-duty required by regulation, falsified their log books, drove more hours in a typical 7-day week, and more frequently had schedules that precluded making on-time delivery without speeding or violating the hours-of-service regulations.

Accid Anal Prev. 2000 Jul;32(4):493-504.

Factors associated with falling asleep at the wheel among long-distance truck drivers.

McCartt AT, Rohrbaugh JW, Hammer MC, Fuller SZ.Institute for Traffic Safety Management and Research, University at Albany, State University of New York, 12205-2604, USA.
preusser@worldnet.att.net

Short time exposure to diesel particulate matter causes inflammation

BrooklynDodger thinks this study helps set an occupational exposure limit to DPM.

"Ten nonsmoking healthy volunteers were exposed for 2 h at rest to a controlled concentration of DEP (monitored at 200 microg/m(3) particulate matter...Levels of exhaled CO were increased after exposure to DEP, and were maximal at 1 h ... There was an increase in sputum neutrophils and myeloperoxidase (MPO) at 4 h after DEP exposure... The investigators concluded that exposure to DEPs leads to an airway inflammatory response in normal volunteers."

The point of departure is an effect level at 200 micrograms for 2 hours at rest, among healthy non smokers for an acute effect. That would be 50 ug/m3 for 8 hours; benchmark dose methods suggest a 10 fold reduction to a no effect level, equivalent to a 10% incidence of airway inflammation. Airway inflammation is a material impairment to health.

Whether this is something special about diesel, or whether it's an effect of small carbon particles remains a subject for debate. BrooklynDodger thinks this is one more example of the effects of particles without other known toxicity at levels previously thought to be orders of magnitude below levels of concern.


VVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVV

Am J Respir Crit Care Med. 2000 Jul;162(1):161-6.

Airway inflammation after controlled exposure to diesel exhaust particulates.

Nightingale JA, Maggs R, Cullinan P, Donnelly LE, Rogers DF, Kinnersley R, Chung KF, Barnes PJ, Ashmore M, Newman-Taylor A.Departments of Thoracic Medicine and Occupational and Environmental Medicine, Royal Brompton Hospital and National Heart and Lung Institute, Imperial College School of Medicine, London, UK.

Epidemiologic evidence suggests a link between morbidity and mortality and levels of particulate matter in the atmosphere.

Overworked and Underpayed Causes Risk Behavior.

Job related psychosocial stress is typically measured by questionaire in the research setting. BrooklynDodger questions whether these instruments are measuring the external work environment or the individuals response to that work environment.

Overworked and underpayed [or otherwise rewarded] is euphemized ["the substitution of an agreeable or inoffensive expression for one that may offend or suggest something unpleasant]" as "effort-reward imbalance." The demand-support-control questions include a series for co-worker support as follows:

[Agree-Disagee]

people are competent in doing their jobs
people take a personal interest in me
people I work with are friendly
people are helpful in getting the job done

The premier long term study of work and health is the Whitehall II study of British public employees. The study regularly produces new findings such as that quoted here:

"...Alcohol dependence of participants in the Whitehall II occupational cohort...was measured ... using the CAGE questionnaire. The psychosocial work environment was measured by self report questions on the job demand-support-control model and on the model of effort-reward imbalance. ... Effort-reward imbalance at work was associated with alcohol dependence in men......Effort-reward imbalance predicted future longstanding illness, poor mental health and negative aspects of close relationships... In women, low decision latitude was related to alcohol dependence to some extent..."

A bad job drives people to drink to excess.

VVVVVVVVVVVVVVVVVVVVVVVVVVVVVV


Occupational and Environmental Medicine 2004;61:219-224

The psychosocial work environment and alcohol dependence: a prospective study

J Head1, S A Stansfeld2 and J Siegrist3
1 Department of Epidemiology and Public Health, University College London, UK2 Department of Psychiatry, Institute of Community Health Sciences, Barts and the London, Queen Mary’s School of Medicine and Dentistry, Queen Mary, London, UK3 Department of Medical Sociology, University of Duesseldorf P.B. 10 10 07 40001, Dusseldorf, Germany

Correspondence to: Ms J Head Department of Epidemiology and Public Health, University College London, London WC1E 6BT, UK; j.head@ucl.ac.uk

Aims: To examine whether a stressful psychosocial work environment predicts alcohol dependence.

[to read the full abstract, go to medline]

Cleaning Up at Lower Cost

Fine particles of ambient compositin at levels permitted by EPA in the community environment, and maybe 10-fold below OSHA occupational limits pose significant health hazards. As industrial hygienists, we reach for the industrial HEPA vacuum cleaner for any mess. This paper indicates that a commercial home cleaner will do just as well.


AIHAJ. 2001 Jul-Aug;62(4):482-93.

Particle emission characteristics of filter-equipped vacuum cleaners.

Trakumas S, Willeke K, Grinshpun SA, Reponen T, Mainelis G, Friedman W.Department of Environmental Health, University of Cincinnati, OH 45267-0056, USA.

Industrial vacuum cleaners with final high-efficiency particulate air (HEPA) filters traditionally have been used for cleanup operations in which all of the nozzle-entrained dust must be collected with high efficiency, for example, after lead-based paint abatement in homes. In this study household vacuum cleaners ranging from $70 to $650 and an industrial vacuum cleaner costing more than $1400 were evaluated relative to their collection efficiency immediately after installing new primary dust collectors in them. Using newly developed testing technology, some of the low-cost household vacuum cleaners equipped with a final HEPA filter were found to have initial overall filtration efficiencies comparable to those of industrial vacuum cleaners equipped with a final HEPA filter. The household vacuum cleaners equipped with a final HEPA filter efficiently collect about 100% of the dry dust entrained by the nozzle. For extensive cleaning efforts and for vacuum cleaning of wet surfaces, however, industrial vacuum cleaners may have an advantage, including ruggedness and greater loading capacity. The methods and findings of this study are applicable to field evaluations of vacuum cleaners.

Lung Disease at the Cleaners

Case reports are an important first step in identifying a hazard associated with an occupational exposure. For metalworking fluids, case reports of asthma in the 1980's, and hypersensitivity pneumonitis in the 1990's lead to more robust scientific work which now recognizes these outcomes as routine in environments in compliance with OSHA standards.

BrooklynDodger expects that this first published association of HP with a solvent exposure will lead to further publications and further study.

As manufacturing industry recedes in the US, a few service industries provide health effects data for common industrial chemicals. Dry cleaning is one of those service industries.

Dry cleaning cohorts in Scandinavia provide the strongest evidence for carcinogenicity of trichloroethylene. A dry cleaning cohort in Oklahoma provides the strongest evidence for carcinogencity of aliphatic hydrocarbon solvents [stoddard solvent.]

IARC gives dry cleaning a 2B, possibly carcinogenic to humans, based on epidemiology:

Variation within individual studies of dry cleaners may depend on the nature and level of exposure, which varies from shop to shop and across studies of dry cleaning workers. There is also variation in the types of solvents used over time and across geographic regions. These limitations notwithstanding, the epidemiological studies on dry cleaning indicate that the risks for cancers at two sites, urinary bladder and oesophagus, may be increased by employment in dry cleaning.

4.3 Other relevant data
Inconsistent evidence of slight renal damage among workers exposed to tetrachloroethylene in dry cleaning shops was found in two studies, whereas two other studies in which exposure to tetrachloroethylene was at least as high did not find such an association.

Disturbances of sperm quality and fertility have been observed among dry cleaning workers in a few studies of limited size. Several studies performed in Nordic countries have shown a consistent increase in the risk for spontaneous abortion among dry cleaners, but the studies are not entirely independent of each other. No effect has been observed on other reproductive outcomes, such as stillbirth, congenital malformation or low birth weight, but the power of the studies was limited.

In single studies, lymphocytes from dry cleaning workers showed no increase in the frequency of alkaline-labile sites/DNA single-strand breaks. There was inadequate information to evaluate the genetic effects in humans of exposures in dry cleaning.

4.4 Evaluation
There is limited evidence in humans for the carcinogenicity of occupational exposures in dry cleaning.

Overall evaluation
Dry cleaning entails exposures that are possibly carcinogenic to humans (Group 2B).

VVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVvv


Respiration. 2004 Nov-Dec;71(6):642-5.

Can we still miss tetrachloroethylene-induced lung disease? The emperor returns in new clothes.

Tanios MA, El Gamal H, Rosenberg BJ, Hassoun PM.Division of Pulmonary, Critical Care and Sleep Medicine, Tufts University School of Medicine, Tufts-New England Medical Center, Boston, MA 02111, USA. mtanios@tufts-nemc.org

Hypersensitivity pneumonitis (HP) is a complex syndrome of varying intensity and clinical presentation, and has been described in association with numerous exposures. Early diagnosis is essential to limit irreversible lung damage. We describe a case of HP in a 42-year-old dry cleaner following occupational exposure to tetrachloroethylene (TCE). The diagnosis was suspected based on clinical presentation and radiographic studies, and confirmed by lung biopsy. A review of the literature reveals that HP has not been reported previously as an occupational lung disease in dry cleaners. We conclude that HP should be suspected in dry cleaners presenting with pulmonary complaints, and TCE should be considered as a potential trigger of disease. The spectrum of TCE-related occupational diseases and the diagnosis of HP are reviewed.

Concentrated Ambient Particles

The particle concentrator gives investigators a chance to observe effects of the particles of composition found in the environment in small groups of people exposed for a short amount of time. In this case, healthy subjects were exposed to small particles at levels ranging above the EPA limit, and 10 fold below the OSHA limit, for two hours. Inflammatory effects were seen, although pathology was not observed. Once again, this is a study powered by concern for community enviromental pollution, the chances of funding for this in the occupational environment is nil.


"Particles were concentrated from the ambient air in Chapel Hill, North Carolina.... Each of 38 subjects was exposed either to filtered air (n = 8) or to CAPs (n = 30) for two hours... For the CAPs-exposed group, the concentration of particulate matter measuring 2.5 microm or less in aerodynamic diameter (PM2.5) in the exposure aerosols varied from 23.1 to 311.1 microg/m3......Subjects exposed to CAPs showed mean increases in fibrinogen of 40 to 48 mg/dL with no obvious differentiation by dose, whereas subjects exposed to filtered air showed no change...... neutrophils showed a dose-dependent increase both when analyzed as an absolute cell count and as a percentage of total lavaged cells. ... We conclude that CAPs induced a modest degree of airway inflammation as judged by lavage, but this effect was not reflected in biopsy tissues from proximal airways. "

VVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVV


Res Rep Health Eff Inst. 2003 Dec;(112):31-50; discussion 51-67.

Health effects of acute exposure to air pollution. Part II: Healthy subjects exposed to concentrated ambient particles.

Holgate ST, Devlin RB, Wilson SJ, Frew AJ.Respiratory Cell and Molecular Biology, Infection, Inflammation and Repair Division, School of Medicine, University of Southampton, Southampton General Hospital, Mail Point B10, Level D, Centre Block, Tremona Road, Southampton SO16 6YD, UK. sth@soton.ac.uk

The purpose of this study was to assess the impact of short-term exposure to concentrated ambient particles ...

[full text of abstract at pub med]

Downsizing and Mortality

First, a process note. BrooklynDodger is going to stop posting the full text of abstracts. They take up a lot of space on the blog, the reader should go find them on medline, which also would yield related references, and those readers who feel out of context postings distort results are encouraged to complain.

A second process note is that the Dodger is not always sure that something hasn't been posted before. But if the Dodger has forgotten writing it, probably the reader has forgotten reading it.

For the last decades, virtually all the work on health impacts of work stress is done in Europe, especially in the Nordic countries and even more in Finland. Researchers in this region can access data not readily available in the US, in this case personnel records and non workers compensation disability insurance.

The workers studied were municipal employees, so the virus of cutbacks in public service seems to have infected European social democracies.

Downsizing stresses employees who survive the cuts because their own jobs are threatened, their work load increases and the quality of their work goes down.

In this study, major downsizing was associated with an increase in sickness absence in permanent employees. More severe downsizing was also associated with more cardiovascular deaths. Cardiovascular mortality was 2.0 (95% confidence interval 1.0 to 3.9) times higher after major downsizing than after no downsizing. A 5.1 times increase in cardiovascular mortality for major downsizing during the first four years after downsizing.

VVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVV

[BMJ articles are available in full text]

BMJ 2004;328:555 (6 March),

Organisational downsizing, sickness absence, and mortality: 10-town prospective cohort study

Jussi Vahtera, senior researcher1, Mika Kivimäki, professor1, Jaana Pentti, statistician1, Anne Linna, research fellow1, Marianna Virtanen, research fellow1, Pekka Virtanen, senior lecturer2, Jane E Ferrie, senior research fellow3

1 Finnish Institute of Occupational Health, Topeliuksenkatu 41 aA, FIN-00250 Helsinki, Finland, 2 University of Tampere, Medical School, FIN-33014 University of Tampere, Finland, 3 International Centre for Health and Society, Department of Epidemiology and Public Health, University College London Medical School, London WC1E 6BT
Correspondence to: J Vahtera, Finnish Institute of Occupational Health, Hämeenkatu 10, FIN-20500 Turku, Finland jussi.vahtera@ttl.fi
"//-->

Objective To examine whether downsizing, the reduction of personnel in organisations, is a predictor of increased sickness absence and mortality among employees.

Depression drives stroke mortality - connecting the dots on job stress and mortality

BrooklynDodger is exploring the link between stress and health. If employment related stress causes depression, and depression causes ill health, then job stress causes ill health. The conclusion requires connecting three dots. Depression has causes other than job stress, increases in job stress may explain only a minority of the variation in depression in the population. It shouldn't be necessary to demonstrate the ultimate health endpoint in a particular study, only the intermediate effect.

In this study, the measure of ill health was dying, specifically from stroke.

The MRFIT project (multiple risk factor intervention and treatment) was one of the those grand and canonical prospective studies of which occupational health researchers can only dream. Probably a hundred papers have come from this data base, which is still being mined.

This study followed people after they exited the trail, correlating later results with the extensive earlier data collected. Changes in these parameters were not measured in the follow up period. It may be that depression at baseline was completely independent of changes in other risk factors (smoking, likely adverse, or alcohol, likely protective) or maybe depressive symptoms drove the other risk factors which in turn drove stroke mortality.

"Men who had completed the Center for Epidemiologic Studies Depression (CES-D) scale (n=11 216) were followed for 18-years... Greater depressive symptoms were associated with significantly higher risk of all-cause mortality and for cause-specific death, a higher risk of CVD, and, more specifically, stroke mortality but not CHD mortality. The significant associations were strongest for those reporting the greatest depression for all-cause mortality,...CVD mortality ... ...stroke mortality ... compared with those in the lowest quintile. These associations were adjusted for age, intervention group, race, educational attainment, smoking at baseline and visit 6, trial averaged systolic blood pressure, alcohol consumption, and fasting cholesterol, as well as the occurrence of nonfatal cardiovascular events during the trial."

(Stroke. 2005;36:98.)© 2005 American Heart Association, Inc.

Depressive Symptoms and Mortality in Men Results From the Multiple Risk Factor Intervention Trial

Brooks B. Gump, PhD, MPH; Karen A. Matthews, PhD; Lynn E. Eberly, PhD; Yue-fang Chang, PhD for the MRFIT Research Group From the Department of Psychology (B.B.G.), State University of New York at Oswego, NY; the Department of Psychiatry (K.M.), University of Pittsburgh, Penn; the Division of Biostatistics (L.E.E.), School of Public Health, University of Minnesota, Minneapolis; and the Department of Epidemiology (Y.C.), University of Pittsburgh, Penn. Correspondence to Dr Brooks B. Gump, Department of Psychology, State University of New York at Oswego, Oswego, NY 13126. E-mail gump@oswego.edu


Background and Purpose— Depression may be a risk factor for cardiovascular disease (CVD) mortality. We evaluated long-term mortality risk associated with depressive symptoms measured at middle age among men at high risk for coronary heart disease (CHD).
Methods— 12 866 men without definite evidence of CHD at study entry but who had above average risk of CHD based on blood pressure, blood cholesterol levels, and/or cigarette smoking were recruited into the Multiple Risk Factor Intervention Trial (MRFIT). Survivors at the end of the trial were followed-up for mortality for an additional 18 years. Men who had completed the Center for Epidemiologic Studies Depression (CES-D) scale near the end of the trial (n=11 216) were used in a prospective analysis of post-trial all-cause and cause-specific mortality during 18-year follow-up after CES-D assessment.
Results— Greater depressive symptoms measured at the end of the trial were associated with significantly higher risk of all-cause mortality and for cause-specific death, a higher risk of CVD, and, more specifically, stroke mortality (all P values <0.02) p="0.48)" hr="1.21" hr="2.03">

The Enemy Within - Guns in the Home

BrooklynDodger has previously posted data showing that the biggest risk of yourself or your family dying by the gun is having one in the house. In addition, you would expect that everyone opposed to further gun control and therefore voting for Bush would have at least one gun at home. This review suggests the upper limit of this problem: about 1/3 nationally, and pushing 50% in the south and Midwest.

The review abstract is paraphrased here and in full text below:

"Published studies indicate that firearms are present in about one third of U.S. households. Handguns in particular are present in more than half of U.S. households with firearms, or about 19% of all U.S. households. The prevalence of firearms and handguns in households with young people was similar to the prevalence overall. The prevalence of firearm ownership was highest in the South, followed by states in the Midwest; firearm ownership in those two regions ranged from 40% to 55%"


vvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvv

Am J Prev Med. 2004 Aug;27(2):173-82.

Firearm ownership and storage practices, U.S. households, 1992-2002. A systematic review.

Johnson RM, Coyne-Beasley T, Runyan CW.Injury Prevention Research Center, School of Public Health, Department of Health Behavior and Health Education, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.

BACKGROUND: Because the presence and improper storage of household firearms are risk factors for injury, it is important to understand the prevalence of ownership and storage practices within households to help guide intervention development. This systematic review of published articles (1992 to 2002) provides prevalence estimates of firearm ownership and storage practices in U.S. households.

METHODS: A search of bibliographic databases (MedLine, CINAHL, PsycInfo, Sociological Abstracts) was completed in January 2003. RESULTS: Although all were cross-sectional, the 42 articles included in this review varied in type; there were seven national and five state prevalence studies, as well as studies using clinic-based convenience samples (n =14) and samples of professionals (n =10). Published studies indicate that firearms are present in about one third of U.S. households. Handguns in particular are present in more than half of U.S. households with firearms, or about 19% of all U.S. households. The prevalence of firearms and handguns in households with young people was similar to the prevalence overall. Firearm ownership was highest in the South.

CONCLUSIONS: Although the methodologic rigor of published articles varies substantially, the literature clearly establishes that firearms are common in U.S. households, even in the homes of medical professionals and those with children.

Hazards of Tight Buildings Documented

BrooklynDodger found a surprisingly strong account of health effects of tight buildings in this study conducted in France.

A tight or air conditioned building presents two hazards to workers within. First, compared to natural ventilation or no mechanical ventilation, air is recirculated so there is dramatically less fresh air. [Taking recirculation into account, calculations based on ventilation manual reference values indicate there is more fresh air in a closet in your house with the door closed than in an air conditioned office.] Vapor phase contaminants, and small particle aerosols - which in France would include tobacco smoke, and perhaps the airborne products of canonical French personal hygiene practices - are endlessly recirculated. Carbon dioxide levels are usually elevated, which may effect regulation of breathing rates.

Somewhat in the direction of less risk, total mold is reduced compared to outside air. However, different mold grows in buildings and the ventilation system than is found in the environment.

A commentary in the journal issue generally concurred on the probability of the effects observed, but remarked on the surprising strength of effect. The commenter put his money on microbial contamination of ventilation systems as the cause.

The abstract is condensed here, and then supplied in full:

"In a national sample of 920 professionally active women aged 49–65 yr ... Being exposed to heating, ventilation, and air-conditioning (HVAC) systems in the workplace proved to be a risk factor for attendance at global and several specialist medical services. The adjusted odds ratio for otorhinolaryngologist attendance was 2.33 ... in the HVAC group compared with the natural ventilation group, and 1.70 ... for sickness absence. Dermatologist and global medical services attendance rates may also be higher in this group. [The investigators concluded that] exposure to HVAC systems was a strong and significant risk factor for otorhinolaryngologist attendance and sickness absence. HVAC systems are prevalent in recent office buildings and have been shown to be associated with several adverse health effects in terms of morbidity and mortality [BrooklynDodger has to look for these references]. "

VVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVV

Workplace air-conditioning and health services attendance among French middle-aged women: a prospective cohort study

P Preziosi1, S Czernichow1, P Gehanno2 and S Hercberg1
1 French Institute of Health and Medical Research (INSERM) Unit 557, UMR (INSERM/INRA/CNAM), Paris, France2 ORL Department, Bichat-Claude Bernard Hospital, Paris, France
Correspondence: S Czernichow French Institute of Health and Medical Research (INSERM) U557, ISTNA–CNAM, 5 rue Vertbois, F-75003 Paris, France. E-mail: sebastien.czernichow@cnam.fr

Objectives To assess the relationship between type of ventilation in the workplace, health services attendance, and sickness absence among middle-aged women.

Methods In a national sample of 920 professionally active women aged 49–65 yr from the SU.VI.MAX cohort, recruited from the general population in France, health services attendance and sickness absence were assessed prospectively during 1999.

Results Being exposed to heating, ventilation, and air-conditioning (HVAC) systems in the workplace proved to be a risk factor for attendance at global and several specialist medical services. The adjusted odds ratio for otorhinolaryngologist attendance was 2.33 (95% CI = 1.35–4.04) in the HVAC group compared with the natural ventilation group, and 1.70 (1.13–2.58) for sickness absence. Dermatologist and global medical services attendance rates may also be higher in this group (P = 0.06 in both cases).

Conclusions Exposure to HVAC systems was a strong and significant risk factor for otorhinolaryngologist attendance and sickness absence. HVAC systems are prevalent in recent office buildings and have been shown to be associated with several adverse health effects in terms of morbidity and mortality. From a public-health perspective, our results outline the need for a quantitative assessment of the health impact of ventilation systems, taking into account the possible loss of production that exists in addition to the direct costs of medical services use.

Getting to First Bayes

Thomas Bayes

BrooklynDodger thought it worthwhile to state the approach of this blog, and also to justify posting a picture gleaned from the web. The Dodger warns the reader that this approach lacks of formal training in either philosophy of science or statistics. "Bayesian" means that the investigator starts with an idea, and a degree of uncertainty that the idea is correct. New pieces of knowledge are sought to strengthen or reduce that degree of certainty.

The blog jumps off from the point of view that occupational and environmental chemical exposures, traumatic injury and musculoskeletal disorder risk factors, and psychosocial stressors are major, abatable causes of illness and injury. Victims are predominantly "innocent" targets of their environment.

The contrary view is that victims are "guilty" of personal behavioral failings or unchangeable genetics. This approach seeks to immunize corporations, governmental and other social forces dominated by the economic elites from responsibility, and thereby preserve the status quo.

So, the Dodger picks scientific and other technical reports which deal with key issues in the debate.

• One issue is that victims behaving badly cause their own illnesses, especially by drinking alcohol and being fat.
• Another issue is that injuries are a product of bad behavior in a satisfactory environment. An example is a one-dimensional [well maybe two dimensional] approach to traffic safety focused only on seat belt use and drunk driving, rather than roads, car design and hours of work.
• Still another is attributing all respiratory cancers to cigarette smoking, by ignoring emerging evidence of many additional respiratory carcinogens.

Alcohol Consumption Protects Against Mortality in the Elderly

Years ago, Peto and Doll attributed 34% of cancer to diet, a canonical number widely quoted today by many authorities actively disinterested in industrial chemicals and pollution as causes of cancer. Doubtless among those dietary causes was alcohol.

Here, Peto and Doll report a 23-year prospective study of 12 000 male British doctors aged 48–78 years in 1978, involving 7000 deaths. …In this elderly population, with mean alcohol consumption per drinker of 2 to 3 units per day, the causes of death that are already known to be augmentable by alcohol accounted for only 5% of the deaths (1% liver disease, 2% cancer of the mouth, pharynx, larynx, or oesophagus, and 2% external causes of death) and were significantly elevated only among men consuming >2 units/day. Vascular disease and respiratory disease accounted for more than half of all the deaths and were both significantly less common among current than among non-drinkers; hence, overall mortality was also significantly lower (relative risk, RR 0.81) …Adding ex-drinkers to current drinkers …still showed that ischaemic heart disease (0.72), respiratory disease (0.69) and all-cause (0.88) mortality were significantly lower than in the non-drinkers.

BrooklynDodger notes that this is a study of the later period of life when the population feels the full force of mortality. That said, even at this age each death avoided is worth 10 years or more to the individual who didn’t die. These reduced relative risks indicate many more lives prolonged than similar reductions among 30 year olds. BrooklynDodger hasn’t reviewed the full text to determine what types of respiratory mortality were reduced among the drinkers.


VVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVVV

http://ije.oupjournals.org/cgi/content/abstract/34/1/199?etoc

International Journal of Epidemiology 2005 34(1):199-204; doi:10.1093/ije/dyh369

Mortality in relation to alcohol consumption: a prospective study among male British doctors

Richard Doll*, Richard Peto, Jillian Boreham and Isabelle Sutherland

Clinical Trial Service Unit and Epidemiological Studies Unit (CTSU), Radcliffe Infirmary, Oxford OX2 6HE, UK

Background To relate alcohol consumption patterns to mortality in an elderly population.
Methods We undertook a 23-year prospective study of 12 000 male British doctors aged 48–78 years in 1978, involving 7000 deaths. Questionnaires about drinking and smoking were completed in 1978 and once again in 1989–91. Mortality analyses are standardized for age, follow-up duration, and smoking, and (during the last decade of the study, 1991–2001) subdivide non-drinkers into never-drinkers and ex-drinkers.
Results In this elderly population, with mean alcohol consumption per drinker of 2 to 3 units per day, the causes of death that are already known to be augmentable by alcohol accounted for only 5% of the deaths (1% liver disease, 2% cancer of the mouth, pharynx, larynx, or oesophagus, and 2% external causes of death) and were significantly elevated only among men consuming >2 units/day. Vascular disease and respiratory disease accounted for more than half of all the deaths and were both significantly less common among current than among non-drinkers; hence, overall mortality was also significantly lower (relative risk, RR 0.81, CI 0.76–0.87, P = 0.001). The non-drinkers, however, include the ex-drinkers, some of whom may have stopped recently because of illness, and during the last decade of the study (1991–2001) overall mortality was significantly higher in the few ex-drinkers who had been current drinkers in 1978 than in the never-drinkers or current drinkers. To avoid bias, these 239 ex-drinkers were considered together with the 6271 current drinkers and compared with the 750 [?misprint, do they mean 7500; that’s the only way to get to 12,000] men who had been non-drinkers in both questionnaires. Even so, ischaemic heart disease (RR 0.72, CI 0.58–0.88, P = 0.002), respiratory disease (RR 0.69, CI 0.52–0.92, P = 0.01), and all-cause (RR 0.88, CI 0.79–0.98, P = 0.02) mortality were significantly lower than in the non-drinkers.

Conclusions Although some of the apparently protective effect of alcohol against disease is artefactual, some of it is real.

Playing with Firearms: injuries among children

BrooklynDodger is back to firearms as a public health issue. This paper
combines public injury data bases. CPSC maintains a data base for injuries
treated in emergency rooms, NEISS. This is even remotely searchable, and
provides a sample of injuries which can be extrapolated to the full nation. The
National Vital Statistics data base provides information on fatalities by cause.

The summary is largely descriptive, although the purpose of quoting it here is to suggest that off-the-job injury
and family safety programs have to address guns, and that gun control efforts
since 1993 have had some success.

“From 1993 through 2000, an estimated 22 661 or 4.9 per 100 000 children
14 years old or younger with nonfatal FA injuries were treated in US
hospital EDs. Assaults accounted for 41.5% of nonfatal FA injuries,
and unintentional injuries accounted for 43.1%. Approximately 4 of
5 children who sustained a nonfatal, unintentional FA injury were
reportedly shot by themselves or by a friend, a relative, or another
person known to them. During this period, 5542, or 1.20 per 100
000 children 14 years old or younger died from FA injuries; 1 of
every 5 children who were wounded by a firearm gunshot died from that
injury. Most FA deaths were violence related, with homicides and
suicides constituting 54.7% and 21.9% of these deaths, respectively.
[For homicides, data on location of incident and person causing the
incident was sparse.] For individuals 14 years old or younger the burden of
morbidity and mortality associated with FA injuries falls
disproportionately on boys, blacks, and children 10 to 14 years old.
Both fatal and nonfatal injury rates declined more than 50% during
the study period.”

^{>>>>>>>>>>>>>>>>>>>>>>>>>>>>}

PEDIATRICS Vol.
113 No. 6 June 2004, pp. 1686-1692

Nonfatal and Fatal
Firearm-Related Injuries Among Children Aged 14 Years and Younger: United
States, 1993–2000

Gabriel B.
Eber, MPH^*, Joseph L. Annest, PhD^*, James A. Mercy, PhD and George W. Ryan, PhD^*

Office of Statistics and Programming,
National Center for Injury Prevention
and Control, Centers for Disease Control and Prevention, Atlanta, Georgia

Division of Violence Prevention, National Center for Injury Prevention and Control,
Centers for Disease Control and Prevention, Atlanta, Georgia

Objective. To provide national
estimates of fatal and nonfatal firearm-related (FA) injuries among children

14
years old and to examine the circumstances under which these injuries occurred.

Methods.
For nonfatal FA injuries among children, we analyzed data on
emergency department (ED) visits from the National Electronic Injury
Surveillance System for 1993 through 2000. National estimates of
injured children who were treated in hospital EDs were examined by
selected characteristics, such as age, gender, race/ethnicity of the
patient, primary body part affected, intent of the injury, the
relationship of the shooter to the patient, where the injury
occurred, and activity at the time of injury. For fatal FA injuries
among children, we analyzed mortality data from the National Vital
Statistics System for 1993 through 2000. Data from both sources were
used to calculate case-fatality rates.

Results.
From 1993 through 2000, an estimated 22 661 (95% confidence interval

[CI]: 16 668–28 654) or 4.9 per 100 000 (95% CI: 3.6–6.2) children

14
years old with nonfatal FA injuries were treated in US hospital EDs.
Assaults accounted for 41.5% of nonfatal FA injuries, and
unintentional injuries accounted for 43.1%. Approximately 4 of 5
children who sustained a nonfatal, unintentional FA injury were
reportedly shot by themselves or by a friend, a relative, or another
person known to them. During this period, 5542, or 1.20 per 100 000
(95% CI: 1.17, 1.23), children

14 years old died from FA injuries; 1 of every 5 children who were
wounded by a firearm gunshot died from that injury. Most FA deaths
were violence related, with homicides and suicides constituting 54.7% and 21.9% of these deaths, respectively. For individuals 14 years old, the burden of morbidity and mortality associated with FA
injuries falls disproportionately on boys, blacks, and children 10 to
14 years old. Both fatal and nonfatal injury rates declined >50%
during the study period.

Conclusions.
Although rates of nonfatal and fatal FA injuries declined during the
period of study, FA injuries remain an important public health
concern for children. Well-designed evaluation studies are needed to
examine the effectiveness of potential interventions aimed at
reducing FA injuries among children

Gout and Alcohol

BrooklynDodger has been fielding some questions of bias, and concedes selective review of the literature on alcohol. After all, it must have some harmful effects. Seeing this title in Lancet, the Dodger figured it was a study of country squires, like Squire Western in Tom Jones. However, the study turned out to be from Boston.

The full abstract is below. The overall incidence of gout in these 47,000 men was 1.5%, which surprised the Dodger. The study covers 12 years, but even so the Dodger would think that someone he knew would have be diagnosed with Gout in that time, but no. Gout increased with beer, spirits, but not with wine consumption. This is one of the first studies to confirm the general assumption that wine is not as bad for you as other types of sauce. [BrooklynDodger usually objects to calling a non significant increase no effect, as was done for wine in this paper, but as a bibulophile choses not to object in this case.

>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
The Lancet Volume 363, Issue 9417 , 17 April 2004, Pages 1277-1281

Alcohol intake and risk of incident gout in men: a prospective study

DrHyon K Choi MDa, d, , , Karen Atkinson MDa, Elizabeth W Karlson MDb, Walter Willett MDc, e and Gary Curhan MDc, d

aRheumatology Unit, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA
bDivision of Rheumatology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA
cChanning Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA
dDepartment of Epidemiology, Harvard School of Public Health, Boston, MA, USA
eDepartment of Nutrition, Harvard School of Public Health, Boston, MA, USA

Available online 20 April 2004.

Summary

Background
The association between alcohol consumption and risk of gout has been suspected since ancient times, but has not been prospectively confirmed. Additionally, potential differences in risk of gout posed by different alcoholic beverages have not been assessed.

Methods
Over 12 years (1986–98) we used biennial questionnaires to investigate the relation between alcohol consumption and risk of incident gout in 47 150 male participants with no history of gout at baseline. We used a supplementary questionnaire to ascertain whether reported cases of gout met the American College of Rheumatology survey gout criteria.

Findings
We documented 730 confirmed incident cases of gout. Compared with men who did not drink alcohol, the multivariate relative risk (RR) of gout was 1·32 (95% CI 0·99–1·75) for alcohol consumption 10·0–14·9 g/day, 1·49 (1·14–1·94) for 15·0–29·9 g/day, 1·96 (1·48–2·60) for 30·0–49·9 g/day, and 2·53 (1·73–3·70) for ≥50 g/day (p for trend <0·0001).>Beer consumption showed the strongest independent association with the risk of gout (multivariate RR per 12-oz serving per day 1.49; 95% CI 1.32-1.70). Consumption of spirits was also significantly associated with gout (multivariate RR per drink or shot per day 1.15; 95% CI 1.04-1.28); however, wine consumption was not (multivariate RR per 4-oz serving per day 1.04; 95% CI 0.88-1.22).

INTERPRETATION: Alcohol intake is strongly associated with an increased risk of gout. This risk varies substantially according to type of alcoholic beverage: beer confers a larger risk than spirits, whereas moderate wine drinking does not increase the risk.