Monday, January 31, 2005

More on Alchohol and Cognition

Let’s face it, those who, like BrooklynDodger, follow the literature on alcohol aren’t that much concerned with what the investigators call “moderate” consumption – one drink a day or maybe two. We have friends who drink a bit more than that [you know how someone goes to a doctor’s office and asks about their “friends’” problems?]

The Dodger figures that the life-prolonging value of moderate drinking – compared to not drinking at all - is a settled question. The evidence for moderate drinking preserving cognition is solid as well, although the recent studies are of women.

Now comes an account of effects of more booze and including guys. The study investigated the relation between alcohol consumption and cognitive function in 4,272 men and 1,761 women. Of people who reported drinking alcohol in the past year, those who consumed at least one drink in the past week, compared with those who did not, were significantly less likely to have poor cognitive function. The beneficial effect extended to those drinking more than 240 g per week (approximately 30 drinks). The effect was stronger for women than men and was not confined to those with evidence of vascular disease. The authors concluded that for middle-aged subjects, increasing levels of alcohol consumption were associated with better function regarding some aspects of cognition.

Four drinks a day is finally a respectable amount.

BrooklynDodger notes that the Whitehall study, covering British public employees, is among the premier data bases in the world regarding class and health status.

A second study was of 4,461 community-dwelling women aged 65-79 years. Compared with no intake, intake of >/=1 drink per day was associated with higher baseline cognition scores and an adjusted odds ratio of 0.40 for significant declines in cognitive function. [Lower risk is better.] Associations with incident probable dementia and mild cognitive impairment were of similar magnitude. Associations with intakes of <1 href="">Alcohol Consumption and Cognitive Function in the Whitehall II Study

Annie Britton, Archana Singh-Manoux, and Michael Marmot
From the International Centre for Health and Society, Department of Epidemiology and Public Health, University College
London, London, United Kingdom.
Received for publication June 26, 2003; accepted for publication February 27, 2004.

The authors investigated the relation between alcohol consumption and cognitive function in a United Kingdom cohort study (4,272 men, 1,761 women) with median follow-up of 11 years. Measures of alcohol consumption were obtained at baseline (1985–1988) and four subsequent phases of data collection. Cognitive function (memory test, AH4, Mill-Hill, phonemic and semantic fluency) was assessed at phase 5 (1997–1999), when participants were aged 46–68 years. Of people who reported drinking alcohol in the past year, those who consumed at least one drink in the past week, compared with those who did not, were significantly less likely to have poor cognitive function. The beneficial effect extended to those drinking more than 240 g per week (approximately 30 drinks). The effect was stronger for women than men and was not confined to those with evidence of vascular disease. Similar associations were found in cross-sectional and longitudinal analyses. The relations were not explained by confounding by smoking and by physical and mental health and, to a large extent, were not mediated by cholesterol or blood pressure. However, the relations were weakened when social position was added to the model. The authors concluded that for middle-aged subjects, increasing levels of alcohol consumption were associated with better function regarding some aspects of cognition. Nonetheless, it is not proposed that these findings be used to encourage increased alcohol consumption.

Am J Epidemiol. 2005 Feb 1;161(3):228-38.

Association between Reported Alcohol Intake and Cognition: Results from the Women's Health Initiative Memory Study.

Espeland MA, Gu L, Masaki KH, Langer RD, Coker LH, Stefanick ML, Ockene J, Rapp SR.

Department of Public Health Sciences, Wake Forest University School of Medicine, Winston-Salem, NC.

Some, but not all, observational studies have suggested that moderate levels of alcohol intake may be associated with improved cognitive function and reduced risk of cognitive decline and dementia. The authors of this 1996-2002 study used data from the Women's Health Initiative Memory Study of postmenopausal combination hormone therapy to assess cross-sectional and prospective associations of self-reported alcohol intake with cognitive function. Across 39 US academic medical centers, 4,461 community-dwelling women aged 65-79 years were followed an average of 4.2 years with annual Modified Mini-Mental State Examinations and standardized protocols for detecting mild cognitive impairment and probable dementia. Compared with no intake, intake of >/=1 drink per day was associated with higher baseline Modified Mini-Mental State Examination scores (p < 0.001) and a covariate-adjusted odds ratio of 0.40 (95% confidence interval: 0.28, 0.99) for significant declines in cognitive function. Associations with incident probable dementia and mild cognitive impairment were of similar magnitude but were not statistically significant after covariate adjustment. Associations with intakes of <1 drink per day were intermediate. Moderate levels of alcohol intake may be associated with better cognition and reduced risk of significant cognitive decline; however, confounding associations with unmeasured factors cannot be ruled out.

Effects of Moderate Alcohol Consumption on Cognitive Function in Women

N Engl J Med 2005;352:245-53.

Sunday, January 30, 2005

Injury Control Going to the Dogs

BrooklynDodger was looking for an off-the-job injury prevention topic which might be more divisive than gun control. The Dodger thinks there is one, summarized below.

The publication below illustrates both a major surveillance data base and the willful ignorance of the hierarchy of controls in the public health community and CDC.

The resource is the National Electronic Injury Surveillance System-All Injury Program (NEISS-AIP). NEISS-AIP is operated by the U.S. Consumer Product Safety Commission and collects data about initial visits for all types and causes of injuries treated in U.S. emergency departments (EDs). NEISS-AIP data are drawn from a nationally representative subsample of 66 out of 100 NEISS hospitals, which were selected as a stratified probability sample of hospitals with a minimum of six beds and a 24-hour ED in the United States and its territories. NEISS-AIP provides data on approximately 500,000 injury- and consumer product--related ED cases each year.

The take home lesson for those who want to refocus occupational programs toward off the job is that the data to do homework on priorities is available. The data quoted in the paper below was only about a year old at the time of publication, which is pretty much real time in the area; anyway, there was no major policy decision hanging on this data, in contrast to the firearms data BrooklynDodger posted recently.

Now, let’s go to the dogs and CDC. BrooklynDodger thinks it isn’t too snarky to complain that the CDC authors have emphasized “education” as the level of control for this type of injury. Not only is education about the lowest level of control, but education for children under the age of 14 in how to act around a dog so the animal won’t bite them. As noted below, it’s the neighbor’s dog which inflicts about half the injuries, followed by the family dog [safer dog, likely longer exposure time.] The Dodger wonders how often the kid got blamed for getting bit?

Nonfatal Dog Bite--Related Injuries Treated in Hospital Emergency Departments --- United States, 2001

MMWR July 4, 2003 / 52(26);605-610

In 2001, an estimated 68 million canines were kept as pets in the United States. An estimated 368,245 persons were treated for dog bites in Emergency Departments. Of these 154,625 (42%) were aged <14>16 years were work-related, including some that occurred while persons were visiting homes as part of their work activities.

CDC in typical fashion opines that prevention programs should educate both children and adults about bite prevention and responsible pet ownership. Additional information about preventing dog bites is available at

Saturday, January 29, 2005

Guns in the Home

The National Safety Council has convinced BrooklynDodger to pay more attention to traumatic injury outside of work. So the Dodger is now going to cover cars and guns, which are pretty prominent in this picture. It would take quite an effort to find something more politically controversial than OSHA, but gun control certainly fills the bill.

CDC investigators concluded that persons with guns in the home were at about twice the greater risk of dying from a homicide in the home. than those without guns in the home. The risk of dying of a firearm homicide at home was 16 fold for persons 35 and older with a firearm in the home. The risk of dying from a suicide in the home was 10 times greater for males in homes with guns than for males without guns in the home. Regardless of storage practice, type of gun, or number of firearms in the home, having a gun in the home was associated with an increased risk of firearm homicide and firearm suicide in the home. Homicide victims were mostly male, less than 35 years of age, and of racial or ethnic minority status. Suicide victims were predominately male, older, and non-Hispanic White.

BrooklynDodger has the impression that the major policy argument by opponents of gun control is greater safety through the possibility of defense of the home against intruders. These data indicate the greatest risk is the enemy already within the home.

BrooklynDodger notes that these data are based on a sample from a 1993 survey, and included about 1500 cases. These data appear to have been sitting around CDC for a while, during which time major legislative debates have taken place on these issues [and presidential elections won and lost.] The Dodger will look for more recent data.

[BrooklynDodger thinks someone could make a living revising abstracts of journal
articles to convey more information. [Actually, isn't that what editors are supposed to do?] For example, the abstract says that "persons" having a gun a home “were also at greater risk of dying from a firearm homicide, but risk varied by age and whether the person was living with others at the time of death.” With no more space they could have conveyed the information from the text: “for persons living with others at the time of death, there was a significant association between the presence of a firearm in the home and risk of a firearm homicide among those aged 35 years or older (adjusted odds ratio = 16.4, 95 percent confidence interval: 5.9, 45.3).” Frankly, we could dispense with “significant association” and say risk was higher [or lower, if the finding were “significant negative association.”]

Abstracts travel the world like a computer virus spread by medline. The full text remains on the journal pay site.

American Journal of Epidemiology 2004 160(10):929-936

Guns in the Home and Risk of a Violent Death in the Home: Findings from a National Study

Linda L. Dahlberg1 , Robin M. Ikeda2 and Marcie-jo Kresnow3

1 Division of Violence Prevention, National Center for Injury Prevention and Control, Centers for Disease Control and Prevention, Atlanta, GA. 2 Epidemiology Program Office, Centers for Disease Control and Prevention, Atlanta, GA. 3 Office of Statistics and Programming, National Center for Injury Prevention and Control, Centers for Disease Control and Prevention, Atlanta, GA.

Data from a US mortality follow-back survey were analyzed to determine whether having a firearm in the home increases the risk of a violent death in the home and whether risk varies by storage practice, type of gun, or number of guns in the home. Those persons with guns in the home were at greater risk than those without guns in the home of dying from a homicide in the home (adjusted odds ratio = 1.9, 95% confidence interval: 1.1, 3.4). They were also at greater risk of dying from a firearm homicide, but risk varied by age and whether the person was living with others at the time of death. The risk of dying from a suicide in the home was greater for males in homes with guns than for males without guns in the home (adjusted odds ratio = 10.4, 95% confidence interval: 5.8, 18.9). Persons with guns in the home were also more likely to have died from suicide committed with a firearm than from one committed by using a different method (adjusted odds ratio = 31.1, 95% confidence interval: 19.5, 49.6). Results show that regardless of storage practice, type of gun, or number of firearms in the home, having a gun in the home was associated with an increased risk of firearm homicide and firearm suicide in the home.
Key Words: firearms; homicide; suicide; violence; wounds and injuries

Friday, January 28, 2005

Chemicals and Work Related Mortality

A bad-guy regulatory deform idea [read OMB] was to require "comparative risk" analysis to support a public health intervention. Is it safer to work in an auto factory, or drive one of their cars? The recent National Safety Council initiative to refocus concerns from on-the-job to off-the-job injury is supported by claims that it's 10 times more dangerous at home.

BrooklynDodger tells people that 90% of identified work-related mortality arises from chronic disease caused by long term exposure to chemicals at work. The abstract quoted in full supports that claim, although this risk contrasts across sectors and job type.

The investigators estimate that 49,000 of 55,000 identifiable work related deaths are form illnesses. The investigators believe, and the Dodger concurs they have biased their estimate conservatively. This is certainly in the 90% ballpark the Dodger uses.

BrooklynDodger advances a few caveats, which would increase these estimates, certainly in some sectors.

First, the estimate across the entire work force underestimates the risk in certain sectors. For the 60% of the workforce who are white collar or professional, or the majority of the workforce in sectors like finance, chemical exposures at work are little different than exposures in the community.

Second, recent observations of respiratory, cardiovascular and carcinogenic risk associated with exposure to particles without special toxicity, imply that previously unrecognized environments put workers at risk.

Both these observations suggest a higher fraction impact of disease in manufacturing, construction and mining, although these are also high risk sectors for traumatic injury.

Thus, for preventing numbers of work related mortality, control of chemical exposures is far more important than traumatic injury prevention [although traumatic injury tends to have a younger age.]

Were cardiovascular effects of noise and work related job stress, and mortality due to depression arising from work related job stress recognized, the proportion of work related to total mortality would rise, although the fraction of work related mortality due to chemicals would fall.

Am J Ind Med. 2003 May;43(5):461-82.

Dying for work: The magnitude of US mortality from selected causes of death associated with occupation.

Steenland K, Burnett C, Lalich N, Ward E, Hurrell J.National Institute for Occupational Safety and Health, Centers for Disease Control and Prevention, Cincinnati, Ohio, USA.

BACKGROUND: Deaths due to occupational disease and injury place a heavy burden on society in terms of economic costs and human suffering.

METHODS: We estimate the annual deaths due to selected diseases for which an occupational association is reasonably well established and quantifiable, by calculation of attributable fractions (AFs), with full documentation; the deaths due to occupational injury are then added to derive an estimated number of annual deaths due to occupation.

RESULTS: Using 1997 US mortality data, the estimated annual burden of occupational disease mortality resulting from selected respiratory diseases, cancers, cardiovascular disease, chronic renal failure, and hepatitis is 49,000, with a range from 26,000 to 72,000. The Bureau of Labor Statistics estimates there are about 6,200 work-related injury deaths annually. Adding disease and injury data, we estimate that there are a total of 55,200 US deaths annually resulting from occupational disease or injury (range 32,200-78,200).

CONCLUSIONS: Our estimate is in the range reported by previous investigators, although we have restricted ourselves more than others to only those diseases with well-established occupational etiology, biasing our estimates conservatively. The underlying assumptions and data used to generate the estimates are well documented, so our estimates may be updated as new data emerges on occupational risks and exposed populations, providing an advantage over previous studies. We estimate that occupational deaths are the 8th leading cause of death in the US, after diabetes (64,751) but ahead of suicide (30,575), and greater than the annual number of motor vehicle deaths per year (43,501). Copyright 2003 Wiley-Liss, Inc.

Wednesday, January 26, 2005

Failed Chemoprevention Study Provides Vital Information about Asbestos and Cancer

BrooklynDodger observes that some studies funded for suspect motives produce results pivotal for public health. For example, the pharma funded clinical trial of VIOXX use against colon polyps [done to increase marketing] revealed, or at least cemented understanding of the dangers overmarketing of COX-2 inhibitors posed to cardiac health. It also may have started a new paradigm about COX's and clotting.

Similarly, the results below are derived from a chemoprevention trial of whether Vitamin A - an antioxidant - protected against future effects of past asbestos [and cigarette smoke] exposure. Among other critics, BrooklynDodger complained that NCI was dumping huge resources into a project that diverted effort from identifying and abating exposure to occupational and environmental carcinogen exposure.

The investigators had enrolled over 4,000 asbestos workers [and a larger number of smokers], screened them at baseline and followed them for over a decade. Recruitment must have been a huge task. Double digit millions must have been spent on this project. In order to measure the impact of the intervention, the investigators had to develop previously unavailable information about the natural history of asbestos and lung cancer.

Previously, the main news from this project was that the chemoprevention study was terminated because Vitamin A increased the risk of lung cancer. BrooklynDodger confesses a certain schadenfreud on hearing that news. Nevertheless, the investigators continued painstaking analysis of results, which they have now published.

The study confirmed excessive rates of lung cancer among men with radiographic asbestosis, but also among workers with no evidence of asbestosis. Among workers with no evidence of asbestosis at baseline, men with more than 40 years' exposure in high-risk trades had a risk approximately fivefold higher than men with 5*10 years. Pleural plaques on the baseline x-ray and abnormal baseline lung function tests were strong independent predictors of subsequent lung cancer.

These results come at a time when asbestos compensation legislation is before the Congress. Frankly, this paper was submitted in February and accepted in August of last year, and might have informed the debate to this point.

The news is a little grim for formerly exposed asbestos workers - even those who exit their trade with a clean x-ray are at increased risk. More thoughts on the implications will follow.

American Journal of Epidemiology 2005 161(3):260-270;

Predictors of Lung Cancer among Asbestos-exposed Men in the ß-Carotene and Retinol Efficacy Trial

Mark R. Cullen1 , Matt J. Barnett2, John R. Balmes3, Brenda Cartmel1, Carrie A. Redlich1, Carl A. Brodkin4, Scott Barnhart4, Linda Rosenstock5, Gary E. Goodman2,6, Sam P. Hammar7, Mark D. Thornquist2 and Gilbert S. Omenn8,9
1 Occupational and Environmental Medicine Program and the Cancer Center, Yale University School of Medicine, New Haven, CT.
2 Fred Hutchinson Cancer Research Center, Seattle, WA.
3 Department of Medicine, University of California School of Medicine, San Francisco, CA.
4 Harborview Medical Center, Seattle, WA.
5 School of Public Health, University of California, Los Angeles, Los Angeles, CA.
6 Swedish Medical Center Cancer Institute, Seattle, WA.
7 Pathology Associates of Kitsap County/Diagnostic Specialties Laboratory, Bremerton, WA.
8 Departments of Internal Medicine and Human Genetics, University of Michigan Medical School, Ann Arbor, MI.
9 Department of Public Health, University of Michigan School of Public Health, Ann Arbor, MI

Despite numerous published studies, debate continues regarding the risk of developing lung cancer among men exposed occupationally to asbestos, particularly those without radiographic or functional evidence of asbestosis. The ß-Carotene and Retinol Efficacy Trial (CARET), a study of vitamin supplementation for chemoprevention of lung cancer, has followed 4,060 heavily exposed US men for 9*17 years. Lung cancer incidence for 1989*2002 was analyzed using a stratified proportional hazards model. The study confirmed excessive rates of lung cancer among men with radiographic asbestosis. Comparison of study arms revealed a strong, unanticipated synergy between radiographic profusion category and the active intervention. In the large subgroup of men with normal lung parenchyma on chest radiograph at baseline, there was evidence of exposure-related lung cancer risk: Men with more than 40 years' exposure in high-risk trades had a risk approximately fivefold higher than men with 5*10 years, after adjustment for covariates. The effect in these men was independent of study intervention arm, but pleural plaques on the baseline radiograph and abnormal baseline flow rate were strong independent predictors of subsequent lung cancer. Residual confounding by subclinical asbestosis, exposure to unmeasured lung carcinogens, or differences in smoking are unlikely to explain these observations better than a carcinogenic effect of asbestos per se.

Key Words: asbestos; asbestosis; beta carotene; clinical trial [publication type]; lung neoplasms; occupational exposure; vitamin A

Copyright © 2005 Johns Hopkins Bloomberg School of Public Health.

Tuesday, January 25, 2005

Coming to work sick is hazardous to your health

Am J Public Health. 2005 Jan;95(1):98-102.

Working While Ill as a Risk Factor for Serious Coronary Events: The Whitehall II Study.

Kivimaki M, Head J, Ferrie JE, Hemingway H, Shipley MJ, Vahtera J, Marmot MG.

Department of Psychology, Finnish Institute of Occupational Health, Topeliuksenkatu 41 aA, FIN-00250 Helsinki, Finland.

Do people who come to work sick suffer an increased incidence of serious coronary events? Analyses were based on a cohort of 5071 male British civil servants without previous myocardial infarction. Absence records were assessed for the 3 years subsequent to baseline screening.
The investigators counted incident nonfatal myocardial infarction or fatal coronary heart disease for an average of 9 years. Seventeen percent of unhealthy employees took no absence during the 3-year follow-up. Their incidence of serious coronary events was twice as high as that of the unhealthy employees with moderate levels of sickness absenteeism. The investigators concluded that employers and employees should be aware of the potential harmful effects caused by coming to work sick.

BrooklynDodger wonders whether the men in this study who stayed home from work when sick also had greater propensity to seek medical care when ill generally, and this prolonged their lives. The Dodger regrets there is no data on women. Women workers are known to suffer more sickness absence while active employees than men, and then live longer after they retire. Some colleagues believe that staying home from work and seeing the doctor when sick may prolong life.

Monday, January 24, 2005

Noise Kills

Occupational exposure to noise causes hearing loss. Ear plugs and muffs don’t sufficiently protect, so that hearing conservation programs [noise measurements, HPD’s and audiograms] primarily measure workers going deaf [maybe more slowly than without the program. Nevertheless, progress on controlling occupational exposure to noise stalls because going deaf isn’t enough of a health effect to induce management to install expensive engineering controls, or even maintain what’s there already. Recent reviews – which BrooklynDodger will post on another day – find that noise exposure causes high blood pressure. High blood pressure in turn causes cardiovascular disease and death. So, noise kills.

The paper sited below provides clear evidence for noise exposure related cardiovacular mortality.

The investigators identified over 27,000 blue-collar workers from lumber mills in British Columbia. Cumulative noise exposure was quantitatively assessed. During the follow-up period, 2510 circulatory disease deaths occurred. Relative risks for acute myocardial infarction mortality were elevated in the full cohort, with a stronger association in the subgroup without hearing protection. There was an exposure-response trend, with a relative risk in the highest exposed group of 1.5. The highest relative risks (2.0-4.0) were observed during subjects' working years. Smoking did not appear to confound these associations. The investigators concluded that chronic exposure to noise levels typical of many workplaces was associated with excess risk for acute myocardial infarction death.

BrooklynDodger points out that the Healthy Worker Effect (HWE) is a huge obstacle to detecting employment related effects on all cause mortality or cardiovascular mortality. In this case, the investigators were able to observe an exposure response trend within the population, which is often the most difficult part of an epidemiologic study.

Making the case for spending money to control noise depends mostly on connecting the dots from diverse studies. Noise causes hearing loss. Hearing protectors don’t work – showing that workers using hearing protectors are exposed to noise. Noise exposure causes high blood pressure. High blood pressure causes cardiovascular disease. However, this study connects the dots.

Epidemiology. 2005 Jan;16(1):25-32.

Occupational exposure to noise and mortality from acute myocardial infarction.

Davies HW, Teschke K, Kennedy SM, Hodgson MR, Hertzman C, Demers PA.

School of Occupational and Environmental Hygiene, University of British Columbia, Vancouver, British Columbia, Canada.

Sunday, January 23, 2005

Get Rich or Die (sooner)

Identification of employment related hazards through mortality studies among workers often hinges on interpretation of the healthy worker effect (HWE). Hourly workers who achieve enough job tenure to get into cohort studies typically enjoy improved mortality experience compared to the general population, yet suffer increased mortality compared to professional and white collar workers in the same industry. African American workers typically show a larger HWE than whites, yet suffer increased mortality compared to white workers in the same enterprise.

The study cited below provides information on that general population to assist interpreting occupational cohort studies.

The investigators calculated mortality differences by socioeconomic status (SES). SES was determined according to the "usual occupation" listed on their death certificates, and were divided into 4 groups. For all-cause mortality, rate ratios from lowest to highest SES quartile for men and women were 2.02, 1.69, 1.25, and 1.00 and 1.29, 1.01, 1.07, and 1.00, respectively. Higher status people were strongly protected from most major causes of death except breast cancer and colorectal cancer. The investigators concluded that mortality differences by SES were sustained through the 1990s and are increasing for men.

BrooklynDodger notes the important public health lesson of this study is the great benefit – nearly two fold - of being in the highest class, compared to the lowest. Class distinction exacts a cost in years of life. Few studies of this type are done and published, perhaps because of their political implications. This study ended observation in 1997. It would be of great value to update this study. The investigators note that these mortality differences are not fully explained by known differences in prevalence of health risk factors by class.

BrooklynDodger thinks this data demands that any occupational cohort mortality study at the minumum stratify on salaried vs. hourly.

For interpretation of occupational cohort mortality studies BrooklynDodger wishes the investigators had devoted more effort to people not usually employed. The investigators observed that 7% of men were not classifiable - unemployed, military, students, volunteers, etc. There are likely additional people who are not usually employed, or on long term disability but whose occupation is noted on death certificate. This 7% might be expected to have even less favorable mortality experience than those who achieved an SES classification in this study. Further, BrooklynDodger expects that persons in lower SES job classification in this study are richer in the marginally employed, persons in the general population but not in occupational cohorts.

All-cause and cause-specific mortality by socioeconomic status among employed persons in 27 US states, 1984-1997.

Am J Public Health. 2004 Jun;94(6):1037-42.

Steenland K, Hu S, Walker J.Department of Environmental and Occupational Health, Rollins School of Public Health, 1518 Clifton Avenue, Atlanta, GA 30322, USA.

Saturday, January 22, 2005

Smoke and Dust Exposure at Work and Cardiovascular Disease

BrooklynDodger quotes below without editing [other than emphasis] a remarkable statement by the experts of one of the mainstream public health organizations in the world. Community exposures at present day levels pose cardiovascular health risks. These community exposures are substantially below those which prevail in the industrial environment. You do the math.

Circulation. 2004 Jun 1;109(21):2655-71.

Air pollution and cardiovascular disease: a statement for healthcare professionals from the Expert Panel on Population and Prevention Science of the American Heart Association.

Brook RD, Franklin B, Cascio W, Hong Y, Howard G, Lipsett M, Luepker R, Mittleman M, Samet J, Smith SC Jr, Tager I; Expert Panel on Population and Prevention Science of the American Heart Association.

Air pollution is a heterogeneous, complex mixture of gases, liquids, and particulate matter. Epidemiological studies have demonstrated a consistent increased risk for cardiovascular events in relation to both short- and long-term exposure to present-day concentrations of ambient particulate matter. Several plausible mechanistic pathways have been described, including enhanced coagulation/thrombosis, a propensity for arrhythmias, acute arterial vasoconstriction, systemic inflammatory responses, and the chronic promotion of atherosclerosis. The purpose of this statement is to provide healthcare professionals and regulatory agencies with a comprehensive review of the literature on air pollution and cardiovascular disease. In addition, the implications of these findings in relation to public health and regulatory policies are addressed. Practical recommendations for healthcare providers and their patients are outlined. In the final section, suggestions for future research are made to address a number of remaining scientific questions.

Hours of Work and Performance: Knock it off or risk injury

BrooklynDodger has been hostile to arguments that reducing overtime, or fatigue associated with work schedule is an important area for prevention of occupational injuries. The Dodger feels that interventions depending on improving worker perception, judgment, reaction time, accuracy, and motivation are limited in impact compared to interventions which abate potential for injury based on engineering controls or substitution.

Nevertheless, within a determined environment, fatigue or other impairments are effect modifiers.

The study referenced below noted that after 17-19 hours without sleep (following a 7+ hour sleep), performance on some tests was equivalent or worse than that at a BAC of 0.05%. Response speeds were up to 50% slower for some tests and accuracy measures were significantly poorer than at this level of alcohol. This corresponds to 9 pm after waking at 6 am. After longer periods without sleep, performance reached levels equivalent to the maximum alcohol dose given to subjects (BAC of 0.1%).

The investigators concluded that these findings reinforce the evidence that the fatigue of sleep deprivation is an important factor likely to compromise performance of speed and accuracy of the kind needed for safety on the road and in other industrial settings.

BrooklynDodger notes that most studies of injury and work duration are based on time into shift rather than time since waking. It is fsbiologically plausible that cognitive effects are more determined by time since waking than work time. This study only measured the acute effects of one day rather than a chronic exposure schedule of 80 hour weeks back to back.

BrooklynDodger notes that when an effect level achieves statistical significance in an exposure-response relationship for adverse effect, the appropriate exposure standard must accommodate an appropriate extrapolation factor to achieve an acceptable level of risk.


Occup Environ Med. 2000 Oct;57(10):649-55.

Moderate sleep deprivation produces impairments in cognitive and motor performance equivalent to legally prescribed levels of alcohol intoxication.

Williamson AM, Feyer AM.School of Psychology, University of New South Wales, Sydney, Australia.

Thursday, January 20, 2005

Alcohol Protects Against Cognitive Decline

BrooklynDodger keeps returning to this theme because of personal concerns, but also out of a contrarian view of blame-the-victim health promotion programs. [Diseases can be stratified on whether they have "innocent" victims or "guilty" victims; for example, Type I diabetics are considered innocent, Type II maybe not so innocent.] Dodger has argued with a major authority that his risk factor rating would give better correlation to health outcomes if he counted "moderate" drinking as a protective factor, not a risk factor.

Anyway, the Nurses Health Study is a great source of data on women's health, although BrooklynDodger points out that it's a special population of women who do physical work, stay up to all hours of the night, and in the Dodger's experience, are pretty assertive in personality.

As with all alcohol studies, BrooklynDodger wonders how much the participants are lying about how much they drink; Dodger always does when filling out health risk appraisals.

Summarizing the abstract [available in full text on medline], the investigators evaluated cognitive function in 12,480 participants in the Nurses' Health Study who were 70 to 81 years old. Moderate drinkers (those who consumed less than 15.0 g of alcohol per day [about one drink]) had better mean cognitive scores than nondrinkers. Among moderate drinkers, as compared with nondrinkers, the relative risk of impairment was 0.77 for general cognition and 0.81 on the basis of a global cognitive score combining the results of all tests . The relative risk of a substantial decline in performance over a two-year period was 0.85 among moderate drinkers, as compared with nondrinkers. There were no significant associations between higher levels of drinking (15.0 to 30.0 g per day) and the risk of cognitive impairment or decline. There were no significant differences in risks according to the beverage (e.g., wine or beer).

NEJM Volume 352:245-253
January 20, 2005
Number 3
Effects of Moderate Alcohol Consumption on Cognitive Function in Women

Meir J. Stampfer, M.D., Jae Hee Kang, Sc.D., Jennifer Chen, M.P.H., Rebecca Cherry, M.D., and Francine Grodstein, Sc.D.

Wednesday, January 19, 2005

For those concerned with the role of NIOSH in the CDC futures project

BrooklynDodger just received a glossy 2005 calendar from CDC, with a letter signed by Julie Gerberding. She wrote: "I hope you will take a few moments to browse through the calendar and gain some insights into our work." The Dodger leafed through the pictures twice, to make sure not to miss anything. Opposite each month there was a glossy picture and some large text words, but there was no glossy picture related to the occupational environment. While March was cited as "Workplace Eye Health and Safety Month," April's observances did not include Worker Memorial Day.

Monday, January 17, 2005

Is Diesel Particulate 100 Times as Carcinogenic as Cigarette Smoke?

It seems bizarre that in 2004 a paper would be published showing that cigarette smoke causes cancer. But this publication actually provides a critical anchor for use of risk assessment from laboratory studies of cancer causing chemicals.

Risk assessment methods debates come back to three questions: Does carcinogenicity at high doses predict risk at lower doses? Does carcinogenicity in laboratory animal studies [usually rats and mice] predict cancer risk in people? And, do high dose studies showing carcinogenicity in laboratory animals [which often cause other physiological changes] predict low dose risk in people?

Critical to the knowledge base supporting risk assessment is examining the behavior of agents known to cause cancer in people, in relation to the results of laboratory bioassays of these chemicals, often bioassays done after the fact of epidemiology.

Most recently, NIOSH asked for comments on whether lab studies of large particle titanium dioxide [found in most white paints] which produced a significant increase in lung tumors in rats at 250 mg/M3 predicted human cancer risk as lower levels. The industry side, predictably, denounced the high exposure levels as being irrelevant to people. A similar debate followed bioassays showing carcinogenicity of diesel particulate matter at much lower levels, 2.5 mg/M3. [Pay attention to the numbers, they are important.] In the case of diesel, the bioassay exposure levels were a small multiple of what workers in indoor settings with diesel engines get, although DPM in the outdoors is closer to 0.005 mg/M3.

The recent paper on cigarette smoke is actually the first bioassay showing clear evidence for carcinogenicity of cigarette smoke in the rat. The investigators reported that male and female F344 rats (n = 81 to 178/gender) [much larger groups than the standard cancer bioassay] were exposed whole-body smoke from 1R3 research cigarettes diluted to 100 mg/M3 (LS) or 250 mg/M3 (HS). There was only a slight reduction of survival at the HS level. Cigarette smoke exposure significantly increased the incidences of non cancer and cancer related proliferative lung lesions in females, while nonsignificant increases were observed in males. The combined incidence of bronchioloalveolar adenomas (benign) and carcinomas (malignant tumors) in females were: HS = 14%; LS = 6%; and C = 0%. The incidence of neoplasia of the nasal cavity was significantly increased at the HS, but not the LS level in both males and females (HS = 6%, LS = 0.3%, C = 0.4% for combined genders).

BrooklynDodger, were we reviewing the papers listed below for publication, would have argued strongly that the abstracts minimize the strength and importance of the findings, to the degree that naive readers will miss their point entirely. BrooklynDodger notes that the lead author has generally argued that risks of DPM to people are low. By contrast, BrooklynDodger points out that simply dividing the effect level for cigarette smoke by the effect level of DPM yields a potency ratio of 100. The lung cancer yield of in people smoking a pack a day is somewhere around 5 to 10%, pretty much the same observed for 250 mg/M3 of cigarette smoke, or 2.5 mg/M3 for diesel particulate matter in the rat.

Toxicol Sci. 2004 Oct;81(2):280-92.

Chronic inhalation exposure to mainstream cigarette smoke increases lung and nasal tumor incidence in rats.

Mauderly JL, Gigliotti AP, Barr EB, Bechtold WE, Belinsky SA, Hahn FF, Hobbs CA, March TH, Seilkop SK, Finch GL.Lovelace Respiratory Research Institute, Albuquerque, New Mexico 87108, USA. jmauderl@lrri.orgA

Fundam Appl Toxicol. 1995 Apr;25(1):80-94.

Comparative pulmonary toxicities and carcinogenicities of chronically inhaled diesel exhaust and carbon black in F344 rats.

Nikula KJ, Snipes MB, Barr EB, Griffith WC, Henderson RF, Mauderly JL.Inhalation Toxicology Research Institute, Lovelace Biomedical and Environmental Research Institute, Albuquerque, New Mexico 87185, USA.

Sunday, January 16, 2005

Flu shots and all that

During the political campaign, BrooklynDodger adopted a riff that went something like this.

"Each election, we try to make occupational health and safety and public and
environmental health an issue. It's pretty much a non starter. During the three
presidential debates, there was only one question on the environment, and public
health discussion limited to simplistic ideas on health promotion discounts for
health insurance premiums. Who would have thought that flu shots would be such a
big deal? Now there's no flu shot for me. Luckily, I live only a tunnel trip to
Canada. Actually, now they are saying that while it's unsafe to bring
prescriptions drugs made in the USA back from Canada, it's safe to take a flu
shot and import the vaccine. I guess that's because the flu vaccine is not made
in an American run plant."

The Dodger never went to Windsor for the shot. But the other day, a radio news story said that CDC had scared and discouraged enough people that there was flu vaccine available to those of us not quite old enough to be high risk. So, BrooklynDodger felt obligated to drive out to our physician’s office to get the shot, so that we can defend our criticism of the abject failure and bungling CDC and FDA as more than a cheap shot. And, the flu season is still here, and not dying of pneumonia was a bit of an incentive.

Seriously, the Administration’s lying, hypocritical and incompetent campaign to terrorize the American public about bioterrorism is most revealed by this debacle on ordinary infectious disease.

After all that, BrooklynDodger learned there are other diseases which might break out. One is RSV, Respiratory Syncytial Virus. Respiratory Syncytial Virus (RSV) is the most common cause of bronchiolitis and pneumonia among infants, and is spread from respiratory secretions through close contact with infected persons or contact with contaminated surfaces or objects. Illness begins most frequently with fever, runny nose, cough, and sometimes wheezing. In adults, it can be really bad.

Another is viral gastroenteritis. Viral gastroenteritis is an infection caused by a variety of viruses that results in vomiting or diarrhea. It is often called the "stomach flu," although it is not caused by the influenza viruses. [Some question whether flu is likely to cause vomiting and diarrhea.] The main symptoms of viral gastroenteritis are watery diarrhea and vomiting. The affected person may also have headache, fever, and abdominal cramps ("stomach ache"). In general, the symptoms begin 1 to 2 days following infection with a virus that causes gastroenteritis and may last for 1 to 10 days, depending on which virus causes the illness. There is now an outbreak in Michigan.

Alcohol and Dementia

Every time BrooklynDodger, now advancing in age, forgets something, certain people express concern about personal habits which may contribute to such lapses. Personal health advice should be evidenced based, so the following report is offered to illuminate such an issue.

The abstract is summarized below. [The full abstract is on medline.]

A cohort of 980 individuals aged 65 and older without dementia at
baseline from New York City [upper west side, not Brooklyn Heights]
were followed annually. After 4 years of follow-up, 260 individuals
developed dementia (199 AD, 61 DAS). Only intake of up to three daily servings
of wine was associated with a lower risk of AD (hazard ratio=0.55). Intake
of liquor, beer, and total alcohol was not associated with a lower risk of AD.

BrooklynDodger was unable to access the full text version
of this paper, so we are unable to comment on the dose response relationship for
this protective effect. Since the biological basis for Alzheimers is not
known, BrooklynDodger is not prepared to discuss the biological
plausibility of these observations.

J Am Geriatr Soc. 2004 Apr;52(4):540-6.

Alcohol intake and risk of dementia.

Luchsinger JA, Tang MX, Siddiqui M, Shea S, Mayeux R.Taub Institute for Research of Alzheimer's Disease and the Aging Brain, and Department of Medicine, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.

Friday, January 14, 2005

Anorexia and Breast Cancer

BrooklynDodger knows there's nothing funny about breast cancer. However, emphasis on lifestyle factors which increase cancer risk can produce ironic results. A recent study reached an expected result that anorexia, as a proxy for severe calorie restriction, was very protective. The investigators studied over 7000 Swedish women hospitalized for anorexia nervosa prior to age 40 years. Compared with the Swedish general population, women hospitalized for anorexia nervosa prior to age 40 years had a 53% lower incidence of breast cancer. Anorexic women who had borne children had a 76% lower incidence. Independently, we know that early childbirth confers protection against breast cancer. Therefore, the lifestyle advice for gaining major protection against breast cancer is anorexia followed by a teenage pregnancy.

JAMA. 2004 Mar 10;291(10):1226-30.

Caloric restriction and incidence of breast cancer.

Michels KB, Ekbom A.Obstetrics and Gynecology Epidemiology Center, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass 02115, USA.

Thursday, January 13, 2005

Extended work hours cause car crashes

For those interested in off the job safety.

This paper demonstrates the off-the-job consequences of extended work hours, in this case, a 3 fold increase in reported motor vehicle crashes.

OSHA and NIOSH and health promotion providers would do well to consider extended work hours as a risk factor as they expend their scarce resources on traffic safety issues. While industrial workers don't often work 24 hour shifts, by comparison to interns, they also don't get to nap on the job during down time either. 80 hour weeks for industrial workers are not that rare.

BrooklynDodger thinks this would certainly be a more productive work-based intervention than telling people to wear their seatbelts and not drive drunk.

[Recent publications also demonstrate increased medical errors arising from these work shifts.]

NEJM Volume 352:125-134 January 13, 2005 Number 2

Extended Work Shifts and the Risk of Motor Vehicle Crashes among Interns

Laura K. Barger, Ph.D., Brian E. Cade, M.S., Najib T. Ayas, M.D., M.P.H., John W. Cronin, M.D., Bernard Rosner, Ph.D., Frank E. Speizer, M.D., Charles A. Czeisler, Ph.D., M.D., for the Harvard Work Hours, Health, and Safety Group

We conducted a prospective nationwide, Web-based survey in which 2737 residents in their first postgraduate year (interns) completed monthly reports that provided detailed information about work hours, work shifts of an extended duration, documented motor vehicle crashes, near-miss incidents, and incidents involving involuntary sleeping.

The odds ratios for reporting a motor vehicle crash and for reporting a near-miss incident after an extended work shift, as compared with a shift that was not of extended duration, were 2.3 and 5.9 respectively. In a prospective analysis, every extended work shift that was scheduled in a month increased the monthly risk of a motor vehicle crash by 9.1 percent and increased the monthly risk of a crash during the commute from work by 16.2 percent.

Tuesday, January 11, 2005

Red Wine Protects Against Prostate Cancer

BrooklynDodger remains skeptical about the general distinction made between protective effect of red wine compared to other forms of alcohol for general mortality. However, there is a biologically plausible hypothesis for why red wine would differ from other forms. Probably not enough white wine drinkers to get significant results.

BrooklynDodger will read the full text to determine if there is any limit to the amount of red wine which confers protection.

International Journal of Cancer
Volume 113, Issue 1 , Pages 133 - 140 (2005)

Alcohol consumption and risk of prostate cancer in middle-aged men

W. Marieke Schoonen 1 2, Claudia A. Salinas 1 4, Lambertus A.L.M. Kiemeney 2 3, Janet L. Stanford 1 4 *

1Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA, USA2Department of Epidemiology and Biostatistics, University Medical Centre Nijmegen, the Netherlands3Department of Urology, University Medical Centre Nijmegen, the Netherlands4Department of Epidemiology, University of Washington, Seattle, WA, USA
email: Janet L. Stanford (

*Correspondence to Janet L. Stanford, Program in Epidemiology, Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave N, M4-B874, Seattle,

Data from a population-based case-control study in King County, WA, were utilized to evaluate the association of alcohol consumption with prostate cancer in middle-aged men.No clear association with prostate cancer risk was seen for overall alcohol consumption. Each additional glass of red wine consumed per week showed a statistically significant 6% decrease in relative risk. No clear associations were seen for consumption of beer or liquor.

Sunday, January 09, 2005

Medical Errors and Work Hours

A prospective, randomized study comparing the rates of serious medical errors made by interns while they were working according to a traditional schedule with extended (24 hours or more) work shifts every other shift while they were working a schedule that eliminated extended work shifts and reduced the number of hours worked per week. Two physicians who were unaware of the interns' schedule assignments independently rated each incident. Interns made 35.9 percent more serious medical errors during the traditional schedule than during the intervention schedule. The total rate of serious errors on the critical care units was 22.0 percent higher during the traditional schedule than during the intervention schedule. Interns made 20.8 percent more serious medication errors during the traditional schedule than during the intervention schedule and 5.6 times as many serious diagnostic errors during the traditional schedule as during the intervention schedule.

Brooklyndodger thinks that if someone designed a work schedule to cause medical errors, you couldn't do much better than current practices in the US health care industry. Instead of cutting off victims' rights to malpractice suits, we suggest President Bush devote some energy to making hospitals attend to issues which create the errors and victims.

N Engl J Med. 2004 Oct 28;351(18):1838-48.
Effect of reducing interns' work hours on serious medical errors in intensive care units.

Landrigan CP, Rothschild JM, Cronin JW, Kaushal R, Burdick E, Katz JT, Lilly CM, Stone PH, Lockley SW, Bates DW, Czeisler CA.Division of Sleep Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA. clandrigan@rics.bwh.harvard.