Monday, June 27, 2005

PM makes the heart go pitter pat

Investigators have found one more data base to crunch to demonstrate the correlation between increases in pollution and cardiovascular effects. In this case, it was the signal from implanted defibrillators.

Patients given implantable cardioverter defibrillators were followed using a case-crossover design to study the association between ambient air pollution and up to 798 confirmed ventricular arrhythmias among 84 [of 203] subjects. The authors found that increases in 24-hour moving average particulate matter less than 2.5 µm in aerodynamic diameter and ozone were associated with 19% and 21% increased risks of ventricular arrhythmia, respectively. For each, there was evidence of a linear exposure response, and the associations appeared independent. These associations were stronger than associations with mean concentrations on the same calendar day and previous calendar days.

American Journal of Epidemiology 2005 161(12):1123-1132

Association of Short-term Ambient Air Pollution Concentrations and Ventricular Arrhythmias

David Q. Rich1,2, Joel Schwartz1,2,3, Murray A. Mittleman2,4, Mark Link5, Heike Luttmann-Gibson1, Paul J. Catalano6,7, Frank E. Speizer1,3 and Douglas W. Dockery1,2,3

1 Department of Environmental Health, Harvard School of Public Health, Boston, MA2 Department of Epidemiology, Harvard School of Public Health, Boston, MA3 Channing Laboratory, Brigham and Women's Hospital and Harvard Medical School, Boston, MA4 Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA5 Tufts-New England Medical Center, Tufts University, Boston, MA6 Department of Biostatistics, Harvard School of Public Health, Boston, MA7 Department of Biostatistical Science, Dana-Farber Cancer Institute, Boston, MA

air pollution; arrhythmias; heart arrest; tachycardia, ventricular; ventricular fibrillation

Tuesday, June 21, 2005

Systemic Effects of Fine Particle Penetration into Systemic Circulation

Another lab paper demonstrates systemic toxicity of PM. Inhalation tox was not available online, so the Dodger can figure the number of particles in the 0.3 u range in the PM 2.5, and therefore a gram to gram extrapolation from this experiment is not appropriate.

Rats were treated using PM2.5 at different dosages (1.5, 7.5, 37.5 mg/kg). Rats were sacrificed 24 h after one-time intratracheal instillation. PM2.5 at dosages of 7.5 and 37.5 mg/kg significantly increased lipid peroxidation levels in the hearts, livers, lungs, and testicles, decreased SOD, CAT, and GPx activities in the lungs, livers, kidneys, and brains, and depleted GSH levels in all the measured organs compared to the control. These results led to a conclusion that airborne PM2.5 was a systemic toxic agent, not only to respiratory and cardiovascular systems. Its toxic effects might be attributed to oxidative damage mediated by prooxidant/antioxidant imbalance or excess free radicals.

Inhalation Toxicology Volume 17, Number 9 / August 2005
Pages: 467 - 473

Effects of Airborne Fine Particulate Matter on Antioxidant Capacity and Lipid Peroxidation in Multiple Organs of Rats

Xiaoli Liu A1 and Ziqiang Meng A1
A1 Institute of Environmental Medicine and Toxicology, Shanxi University, Taiyuan, China

Tuesday, June 14, 2005

Disrespecting People Who Work with their Hands as Well as Their Heads

Sometimes a newspaper article acquires such bogosity that it must enter a science blog. This op-ed column, aimed at softening up voters for an older retirement age, suggests putting off retirement to "work at the office." The majority of Americans work in executive, professional, sales, technical and administrative jobs. But a substantial minority - and those who make and build stuff rather than sell it - have jobs with serious physical demands. People who pound steel on the assembly line 10 hours a day and didn't have time or energy to pump iron or train for the marathon.

There's a lot of population literature suggesting musculoskeletal problems for older people with "physically demanding" jobs, but it's mostly questionaire job data which doesn't distinguish seriously repetitive or heavy work. It's time to compile that literature before we condemn people to another 10 years doing more than the body can stand.

Op-Ed Columnist
The Old and the Rested

Published: June 14, 2005

Men in their 70's raced on bikes for 40 kilometers in this month's National Senior Games in Pittsburgh. A 68-year-old woman threw the discus 85 feet, and a 69-year-old man hurled the javelin nearly half the length of a football field.

Is it possible that people this age are still physically capable of putting in a full day's work at the office?

Monday, June 13, 2005

Fine Particles and Cardiovascular Mortality - Ignored by Occupational Health Practitioners

Microgram for microgram, particulate air pollution is way more toxic than cigarette smoke. The cig exposure is way higher.

Once again, an exposure response relationship for actual death which starts well below the prevailing exposure levels in American manufacturing workplaces.

Circulation. 2004 Jan 6;109(1):71-7. Epub 2003 Dec 15.

Cardiovascular mortality and long-term exposure to particulate air pollution: epidemiological evidence of general pathophysiological pathways of disease.

Pope CA 3rd, Burnett RT, Thurston GD, Thun MJ, Calle EE, Krewski D, Godleski JJ.Brigham Young University, 130 FOB, Provo, UT 84602-2363, USA.

Vital status, risk factor, and cause-of-death data, collected by the American Cancer Society as part of the Cancer Prevention II study, were linked with air pollution data from United States metropolitan areas. Cox Proportional Hazard regression models were used to estimate PM-mortality associations with specific causes of death. Long-term PM exposures were most strongly associated with mortality attributable to ischemic heart disease, dysrhythmias, heart failure, and cardiac arrest. For these cardiovascular causes of death, a 10-microg/m3 elevation in fine PM was associated with 8% to 18% increases in mortality risk, with comparable or larger risks being observed for smokers relative to nonsmokers. Mortality attributable to respiratory disease had relatively weak associations.

CONCLUSIONS: Fine particulate air pollution is a risk factor for cause-specific cardiovascular disease mortality via mechanisms that likely include pulmonary and systemic inflammation, accelerated atherosclerosis, and altered cardiac autonomic function. Although smoking is a much larger risk factor for cardiovascular disease mortality, exposure to fine PM imposes additional effects that seem to be at least additive to if not synergistic with smoking.

Sunday, June 12, 2005

Behavior Based Safety at NASA

Sometimes a news story comes close enough to public health to justify BrooklynDodger posting it to the science site. Hidden in the NY Times article on a NASA shakeup was:

NASA has also canceled a consulting contract with a company hired to improve what the board investigating the Columbia shuttle disaster called the "broken safety culture" in which managers played down risks and squelched dissent. The company, Behavioral Science Technology, based in Ojai, Calif., conducted more than 300 surveys in NASA's centers and led behavioral training.

Mr. Mirelson said that the company had served its purpose and "the input has been, obviously, invaluable," but that future efforts would be within NASA. The company did not return calls seeking comment.

Many NASA employees have said the training is unhelpful. In an interview in April, Dr. Charles J. Camarda, an astronaut who will fly in the mission of the shuttle Discovery, called it "charm school" and said such efforts "are not going to change the culture."

The BST website will probably still list NASA as a client. Maybe they should take down BP Amoco, after the Texas City catastrophe.

Sunday, June 05, 2005

Staph Infections Taken Home

MRSA was identified from the nasopharyngeal swabs of 87 HCWs, collected one to two weeks after contact with 592 known MRSA-positive patients. These HCWs were withdrawn from work and treated with topical antibiotics/antiseptics. They were screened for successful eradication for up to three months. Seventy-three (84%) HCWs lost their carrier status. The eradication regimen failed in 14 cases. In 11 of these MRSA was detected only in later nasopharyngeal swabs (suspected recolonization). Screening identified nasal colonization of close household contacts in eight of these 11 cases. Environmental sampling detected contamination in seven out of eight screened home environments. When eradication treatment was applied to household contacts and when household surfaces were cleaned and disinfected, the carriage cleared in most cases within a few weeks. However, when home environments are heavily contaminated, despite adequate medical treatment, eradication took up to two years.

Hosp Infect. 2005 Mar;59(3):180-7.

Bed, bath and beyond: pitfalls in prompt eradication of methicillin-resistant Staphylococcus aureus carrier status in healthcare workers.

Kniehl E, Becker A, Forster DH.ZLMT, Department of Microbiology and Infection Control, Klinikum Karlsruhe, Moltkestr.

A Rash of Papers on Bacterial Contamination of Surfaces

The Dodger found a rash of papers on bacterial contamination on surfaces. Quantitative exposure response relationships, and then assessment of exposure, is the way forward in designing performance oriented methods for infection control. The point here is that we live in a world swarming with bacteria, especially children, and people don't get sick from the normal fauna around us.

About 1000 environmental surfaces [what other kind of surfaces are there?] from shopping, daycare, and office environments, personal items, gymnasiums, airports, movie theaters, restaurants, etc.), in four US cities, was [were] monitored. ...Biochemical markers, i.e., hemoglobin (blood marker), amylase (mucus, saliva, sweat, and urine marker), and urea (urine and sweat marker) were detected on 3% (26/801); 15% (120/801), and 6% (48/801) of the surfaces, respectively. Protein (general hygiene marker) levels ??200?µg/10?cm 2 were present on 26% (200/801) of the surfaces tested. Surfaces from children's playground equipment and daycare centers were the most frequently contaminated (biochemical markers on 36%; 15/42 and 46%; 25/54, respectively). Surfaces from the shopping, miscellaneous activities, and office environments were positive for biochemical markers with a frequency of 21% (69/333), 21% (66/308), and 11% (12/105), respectively). Sixty samples were analyzed for biochemical markers and bacteria. Total and fecal coliforms were detected on 20% (12/60) and 7% (4/60) of the surfaces, respectively. Half and one-third of the sites positive for biochemical markers were also positive for total and fecal coliforms, respectively. Artificial contamination of public surfaces with an invisible fluorescent tracer showed that contamination from outside surfaces was transferred to 86% (30/35) of exposed individual's hands and 82% (29/35) tracked the tracer to their home or personal belongings hours later.

Occurrence of bacteria and biochemical markers on public surfaces
Reynolds, Kelly 1; Watt, Pamela 2; Boone, Stephanie 1; Gerba, Charles 1

International Journal of Environmental Health Research, June 2005, vol. 15, no. 3, pp. 225-234

1: Department of Soil Water and Environmental Science, The University of Arizona, Tucson, Arizona 2: US Department of Agriculture, Agricultural Research Service, Riverside, California, USA

Saturday, June 04, 2005

DWM - Classics in Epidemiology and Statistics

BrooklynDodger was ADDing on the question of epidemiological evidence for causation when the Dodger made three discoveries. We all refer to the "Bradford Hill" "criteria." First, the "A" in Bradford Hill stands for Austin, not Arthur. Second, while this paper reads like a Brit after dinner speach at some meeting, it was the Presidential Address to the Occupational section of the British Medical Association. Third, Sir Austin was trained as an economist, he never went to epidemiology school.

The actual text of this address is hard to get in full text because it goes back to 1965, actually not so long ago.

"On fair evidence we might take action on what appears to be an occupational hazard, e.g. we might change from a probably carcinogenic oil to a noncarcinogenic oil in a limited environment and without too much injustice if we are wrong. But we should need very strong evidence before we made people burn a fuel in their homes that they do not like or stop smoking the cigarettes and eating the fats and sugar that they do like [1](p.300)."

So present day public health has pretty much 180'd this prescription. OSHA has refused to reduce the exposure limit for metalworking fluids in the face of consensus that asthma and HP appear with greater frequency when exposures exceed 0.5 mg/M3 [compared to a current limit of 5], and a dozen studies showing increased mortality from cancer at a variety of sites. Meanwhile, all the energy is going into health risk behavior, without much of a clue as to how to change that behavior.

For historical value, references to the first studies proving increased risk for lung cancer from cigarettes are reproduced below.

The missed lessons of Sir Austin Bradford Hill

Carl V Phillips1, 2, 3 and Karen J Goodman1

1Management, Policy and Community Health Division, University of Texas School of Public Health, 1200 Pressler, Houston, TX 77225, USA2Center for Clinical Research and Evidence-Based Medicine, University of Texas Medical School, Houston, TX USA3Center for Philosophy, Health, and Policy Sciences, Inc, Houston, USA

Epidemiologic Perspectives & Innovations 2004, 1:3

Doll R, Hill AB. The mortality of doctors in relation to their smoking habits. Br Med J 1954;228:1451-5. Reproduced in: BMJ 2004;328:1529-3.

Doll R, Hill AB. Lung cancer and other causes of death in relation to smoking. A second report on the mortality of British doctors. BMJ 1956;233:1071-6.

Doll R, Peto R, Boreham J, Sutherland I. Mortality in relation to smoking: 50 years' observation on male British doctors. BMJ 2004;328:1519-33.