Tuesday, April 26, 2005

Foot, Ankle, Knee and Work

Many people report "lower extremity" problems from work, but chronic problems are rarely if ever reported in official statistics or recorded on the OSHA 300. BrooklynDodger was surfing medline, and found this early data mining effort from the Framingham study.

In this study, knee osteroarthritis (OA) was assessed by weight bearing knee radiograph at when mean age of subjects was 73 years. Each subject's job was characterized by its level of physical demand and whether the job was associated with knee bending. Men whose jobs required knee bending and at least medium physical demands had higher rates of later radiographic knee OA (at least definite osteophytes) than men whose jobs required neither (43.4 vs 26.8%; OR of OA = 2.22) Rates of severe radiographic OA (osteophytes and joint space narrowing) and of bilateral radiographic OA were also significantly increased in these men.


Occupational physical demands, knee bending, and knee osteoarthritis results from the Framingham Study

Felson, D. T.; Hannan, M. T.; Naimark, A.; Berkeley, J.; Gordon, G.; Wilson, P. W., and Anderson, J. .
J Rheumatol. 1991 Oct; 18(10)1587-92.

Sunday, April 24, 2005

Color vision and solvents

This report is one of several looking for neurobehavioral effects of organic vapor exposures at levels below recommended exposure limits. Early on, occupational health investigations attempted to cobble together various computer based variants of psychological tests as measures of impacts. The paper and pencil versions were likely validated in some way, at least large numbers of people took them. Computer based versions were less widely used. A long review would be needed to compare solvent effect levels with alcohol, psychoactive medication, sleep deprivation and other modifiers. BrooklynDodger opines that these test batteries are insensitive to substantial effects, and would have little impact on allowable exposure to solvents.

The report below goes another way: instead of examining variation in complex cognitive functions, why not look at very precise effects on the sensory apparatus.

Effects of styrene on color vision have been published before.

In paraphrase of abstract, styrene exposure and color vision was studied at Swedish reinforced plastic plants. Current exposure varied between 0.3 and 96 mg/m3. Cumulative past exposures varied from 18 to 4455 mg years/m3, and an index of lifetime weighted average exposure varied from 5 to 129 mg/m3. ... Analyses of variance revealed effects color vision. This study thus indicates that styrene exposure even at levels below the current Swedish OEL of 20 mg/m3 may affect color vision negatively.

The OSHA PEL for styrene is 100 ppm or 420 mg/M3. The ACGIH TLV is 50 ppm or 210 mg/M3. For risk assessment purposes, a decision whether hurting color vision is a central nervous system effect on higher and more conferning nervous system function.


Environmental Toxicology and Pharmacology Volume 19, Issue 3 , May 2005, Pages 511-516

Low-level styrene exposure and color vision in Swedish styrene workers

Anders Iregrena, , , Ann-Christin Johnsonb, c and Per Nylénd a

National Institute for Working Life, Risk Assessment Group, Box 210, SE-171 77 Stockholm, SwedenbKarolinska Institute, Unit of Audiology, Department of Clinical Science, Stockholm, SwedencNational Institute for Working Life, Work and the Physical Environment, Umeå, SwedendNational Institute for Working Life, Department of Ergonomics, Stockholm, Sweden Available online 3 February 2005.

Saturday, April 23, 2005

Overweight Promotes Health - Take That Tommy Thompson

BrooklynDodger continues to opine that the CDC campaign on obesity is an opening salvo attacking health insurance benefits. People who get sick are guilty victims of their inability to control their appetites. The attack does collateral damage by minimizing importance of environmental and social pollution, and denial of quality medical care.

The recent paper contradicting this campaign comes from the scientific branch of CDC, and is available in full text from JAMA. Even so, the authors bury their main finding in the abstract:

"Overweight was not associated with excess mortality (–86 094 deaths; 95% CI, –161 223 to –10 966). "

[The full text of the abstract is reproduced below, to enable the reader to draw the reader's conclusions on distortion].

BrooklynDodger is mystified why an author would write "not associated with excess mortality" when the actual result is a decrease in mortality which is statistically significant. Most of the words are devoted to obese vs. normal, rather than overweight vs. normal.

For a six foot tall person, 135 lbs borders underweight, 185 borders overweight, and 235 borders obese. In this survey, barely 1/3 of the population was of "normal" weight. The benefits of "overweight" compared to "normal" were greater among non-smokers. The study took smoking into account, since lower weight strata are richer in smokers than higher strata. BrooklynDodger would not be surprised if there were something unhealthy in 6 foot persons weighing less than 135 lbs.

BrooklynDodger thinks the op-ed piece below misses the boat. It's not moralism and scolding which has driven the latest campaign. The motivation is more pernicious. It's a campaign to blame victims, to promote removing benefits from victims.


Excess Deaths Associated With Underweight, Overweight, and Obesity

Katherine M. Flegal, PhD; Barry I. Graubard, PhD; David F. Williamson, PhD; Mitchell H. Gail, MD, PhD

JAMA. 2005;293:1861-1867

Results Relative to the normal weight category (BMI 18.5 to <25),>



Fat and HappyBy JOHN TIERNEY

Published: April 23, 2005

Friday, April 22, 2005

Traffic Fatalities - A National Endemic

BrooklynDodger vacillated on whether this was personal or scientific, and has opted to snark on the National Safety Council and DOT in the scientific arena.

First, the Dodger must complain that a condition which is more or less the same all the time is "endemic" not "epidemic." Endemic conditions likely do more damage than epidemic. This is slovenly terminology, like conflating acute [short term] with "really bad."

Second, the Dodger questions whether issuing a preliminary account, to be followed by a final account alleged to have the same data, is merely a twofer for press release purposes.

Next comes the interpretation, particularly the highlighting of the seat belt issue, and drunk driving which didn't get mentioned. The DOT report is available as a powerpoint at http://www-nrd.nhtsa.dot.gov/pdf/nrd-30/NCSA/PPT/2004EARelease.pdf

For 2004, it's projected there will be 42,000 motor vehicle fatalities. Fatilities are trending down, except for motorcycles and heavy trucks, which are going up.

44% of vehicle occupants killed were wearing seatbelts. This suggests some limits in seatbelts as a total strategy. Alcohol was found in 39% of fatalities [assuming mostly the driver]. Some fraction of these alcohol related fatalities were caused by the same factors which caused the 61% unrelated. Speeding was identified in 31% of fatalities.

Preliminary efforts at parsing the FARS data base suggests confounding of drunk driving and not wearing seat belts. The high fatality times are weekend nights. Probably speeding is confounded with drunk driving and not wearing seatbelts. Younger drivers are at increased risk. Together this suggests that interventions aimed at mature drivers going to work in daylight will do little to reduce fatalities.

Among the 5100 killed in heavy truck incidents, 750+ were in the heavy truck and the other
4000 were in the light vehicle. About 16% of the total. This rate went up 4% for total victims. For trends, heavy truck is trending up, and light vehicle only incidents are trending down. Likely seat belts are less effective in crashes between light vehicles and heavy trucks.


Mineta: Highway traffic fatalities ‘national epidemic’

On April 21, Transportation Secretary Norman Y. Mineta announced “mixed results” in the effort to reduce the number of people killed on U.S. highways. Although the fatality rate dropped and alcohol-related crashes were down from 2003, 42,800 people died on the nation’s highways in 2004 – up slightly from 42,643 in 2003, according to projected 2004 data compiled by NHTSA in a preliminary report. The report also projects the seventh straight increase in motorcycle fatalities.

Mineta called the number of fatalities a “national epidemic,” and said, “If this many people were to die from any one disease in a single year, Americans would demand a vaccine. The irony is we already have the best vaccine available to reduce the death toll on our highways – safety belts.”

Tuesday, April 19, 2005

Smoking Increases Health Care Costs - A contrary view

Recently BrooklynDodger posted a paper based on Netherlands data which stated that smoking cessation caused short term savings in health care costs, but after 15 years or so caused an increase in costs through smokers not dying early.

To repeat, the issue is whether increasing health care insurance costs are due to bad habits of the disease victims, or whether healthier behaviors will reduce costs.

This more recent analysis, using Danish data, concluded "Annual direct and indirect costs of ever-smokers were higher than for never-smokers in all age groups of both genders. ... Taking life expectancy differences into account, direct and indirect lifetime health costs for men aged 35, discounted by 5% per year were 66% and 83% higher in ever-smokers than in never-smokers. Corresponding results for women were 74% and 79%, respectively. ... Excess costs of ever-smokers disappear if the inclusion of smoking-related diseases is narrowed to that of previous studies."

BrooklynDodger is just a simple country toxicologist, so these complex economic considerations are difficult to parse. The Dodger think the take home lesson is that health care cost impact for smoking cessation is a close call, depending on methods and assumptions. However, neither the Dutch study before, or the Danish study now, took into account the pension savings from early death.

Obviously the victims pay, regardless of whether the social insurance scheme or the employers benefit or not.


Eur J Public Health. 2004 Mar;14(1):95-100.

The total lifetime costs of smoking.

Rasmussen SR, Prescott E, Sorensen TI, Sogaard J.
DSI Danish Institute for Health Services Research, Copenhagen, Denmark. srr@dsi.dk

Sunday, April 17, 2005

Smoking - Cost Benefit Reduced to Absurdity

BrooklynDodger has maybe blogged that the rash of CDC pronouncements about the "epidemic" of obesity was an early barrage to soften opposition to cutting medicare and medicaid benefits. Smoking has recently appeared in a series of attacks on employee health insurance benefits in the news media.

Don't mistake the Dodger's point here - the Dodger thinks everyone who now smokes should never have started and should stop now. [And not having this habit to kick, everyone now overweight to start exercising and lose weight, not so easy to do sitting at the computer].

The adverse impact of smoking on health care costs is not as clean as people assume. That's because a lifetime insurance system makes money on early death.

Based on Netherlands numbers, the investigators concluded: Health care costs for smokers at a given age are as much as 40 percent higher than those for nonsmokers, but in a population in which no one smoked the costs would be 7 percent higher among men and 4 percent higher among women than the costs in the current mixed population of smokers and nonsmokers. If all smokers quit, health care costs would be lower at first, but after 15 years they would become higher than at present. In the long term, complete smoking cessation would produce a net increase in health care costs.

These estimates ignore the savings to pensions from early death. This cost benefit also assumes that quitting smoking is free.

The important take home lesson goes beyond victim blaming. Life saving interventions will mostly fail a cost benefit test from an employer perspective: pension savings and retiree health insurance savings from early death will outweigh the cost of providing protection.


N Engl J Med. 1997 Oct 9;337(15):1052-7.

The health care costs of smoking.

Barendregt JJ, Bonneux L, van der Maas PJ.Department of Public Health, Erasmus University, Rotterdam, the Netherlands.

Saturday, April 16, 2005

The Shelby Amendment - Massive Theft of Intellectual Property of Environmental Health Investigators

The "Shelby Amendment" advanced the bad guy counterattack to the Harvard Six Cities Study. The Amendment, and the OMB Circular A-110 which implemented the legislation, are dissected at the site below:


This amendment was a direct result the attack on EPA regulation on clean air. [Others think it may be aimed at CDC studies of firearm fatalities. In any event, it was without doubt a bad guy idea.] The Harvard Six Cities study was NIH funded.This data that was used by the EPA in writing the particle rule. Industry forces fighting the EPA rule wanted the underlying data that Harvard had generated so they could re-analyze it and criticize the EPA regulatory policy. EPA publicly provided aggregated data used in its risk assessment and cost-benefit analysis, but did not provide the underlying information which was retained by Harvard.

The FOIA applies to data in government hands. Data in the hands of private institutions was not subject to FOIA prior to the Shelby Amendment and OMB's A-11o amendments.

The rule makes "research data relating to published research findings produced under an award that were used by the Federal Government in developing an agency action that has the force and effect of law" publicly accessible under the procedures of the Freedom of Information Act. Only data produced by nonprofit grantees, and not data from contractors is covered.

Think of this in personal terms. A researcher toils for years to produce data deemed important to protect public health by the funding agency. The researcher risks these career years coming up empty. A research career depends on important results published. Now, an idea pans out, it's important. All of a sudden, the full force of industry which is impacted by the scientific results comes out.

Now comes the unoriginal researcher, bankrolled by industry, not peer reviewed or qualified by the study section, to the original researcher, and says "give me your work product." Even if time and effort are paid for, time and effort of scientists on turning over files brings negative career rewards. Nobody ever got tenure for running a xerox machine. Because the original result was important enough for publication, the unoriginal analyses will be publishable.

To rub salt, research by for profit contractors is exempt, only research by non-profit grantees is covered. Industry sponsored "money tox" is completely exempt.

BrooklynDodger will blog on the reanalysis of the Six Cities study later.

Thursday, April 14, 2005

Mental Illness Doesn't Cause Cancer

Apparently there is another population prospective health study, the Swedish Twin registry. Twins studies reduce or eliminate genetic factors, although twins may experience hightly correlated environments. In this study of 29000 twins [14000 pairs?], A personality test measured neuroticism and extroversion. All analyses were conducted for six etiologically different groups of cancers: hormone-related organ cancers, virus-related and immune-related cancers, digestive organ cancers (excluding liver), respiratory organ cancers, cancers in other sites, and all cancer sites. The authors found no significant association between neuroticism, extroversion, their joint effects and the risk for any cancer group.

Cancer. 2005 Mar 1;103(5):1082-91.

Personality traits, health behavior, and risk for cancer: a prospective study of Swedish twin court.

Hansen PE, Floderus B, Frederiksen K, Johansen C.Department of Psychosocial Cancer Research, Institute of Cancer Epidemiology, The Danish Cancer Society, Copenhagen, Denmark. pernille@cancer.dk

Tuesday, April 12, 2005

Cell Phones and Brain Cancer

Here's a null study more interesting for the acknowledgements than the study itself. This cell phone deal won't die because it's a yuppie exposure; true, other people are exposed as well, but this is one of the few environmental issues where money tox for the exposed people.

The fear of association of brain cancer with electrical phenomena metaphors "brain waves" into a biologically implausible connection. Yes, nerve cells operate by conducting a membrane based impulse down the axon, yes, the electrical activity can be measured, and yes, brain and nervous system activity are disrupted by electric shock. Measurable electrical potentials are generated by lots of cells, especially muscles like the heart. But CNS tumors have little to do with the neurons, which basically don't divide and grow. CNS tumors arise from glial cells which wrap around the neurons and nurture the neurons. Another class of CNS tumors, meningiomas, arise from the membrane wrapping the CNS.

It's certainly reasonable to wonder whether sticking a radio transmitter on the side of your head might carry some biological effect. But if the Dodger were investigating this, the first step would be measuring the exposure. Maybe this has been done.

Anyway, a paraphrased abstract of the study notes The authors ascertained all incident cases of glioma and meningioma diagnosed in Denmark for two years, 252 persons with glioma and 175 persons with meningioma. Use of cellular telephone was associated with a low risk for high-grade glioma (OR, 0.58) The risk estimates were closer to unity for low-grade glioma (1.08) and meningioma (1.00).

More intersting is the acknowledgement section. The International Epidemiology Institute is a private consulting group in a modest office building in Rockville; where IEI gets the money to "sponsor" studies mystifies the Dodger. Rare are the sudies published by the IEI investigators which find an environmental or occupational cause of cancer. The rest seems to be paid for by the cell phone industry.

NEUROLOGY 2005;64:1189-1195

Cellular telephones and risk for brain tumors

A population-based, incident case-control study

H. Collatz Christensen, MD, J. Schüz, PhD, M. Kosteljanetz, DMSc, MD, H. Skovgaard Poulsen, DMSc, MD, J. D. Boice, Jr, ScD, J. K. McLaughlin, PhD and C. Johansen, PhD, DMSc, MD
From the Institute of Cancer Epidemiology (Drs. Collatz Christensen and Johansen), The Danish Cancer Society, Denmark; Institute for Medical Biostatistics, Epidemiology and Informatics (Dr. Schüz), University of Mainz, Germany; Neurosurgical Department (Dr. Kosteljanetz) and Oncological Department (Dr. Skovgaard Poulsen), University Hospital of Copenhagen, Denmark; and International Epidemiology Institute (Drs. Boice and McLaughlin), Rockville, MD.
Address correspondence and reprint requests to Dr. H. Collatz Christensen, Institute of Cancer Epidemiology, Danish Cancer Society, Strandboulevarden 49, DK-2100 Copenhagen, Denmark; e-mail: hcollatz@dadlnet.dk

Supported by the European Commission Fifth Framework Program—Quality of life and management of living resources (Contract QLK4-CT1999–01563), a grant from Union Internationale Contre le Cancer (UICC) (RCA/01/08), a grant from the International Epidemiology Institute, Rockville, MD, and the Danish Cancer Society. The UICC received funds for this purpose from the Mobile Manufacturers' Forum and the GSM Association.

Monday, April 11, 2005

The ACS study of air pollution and mortality

The second major finding hit the press in 1995: an American Cancer Society study of half a million Americans in 151 cities. Detailed data on individuals was less than the Harvard 6 Cities study, but the breadth of data were overwhelming.

Paraphrased abstract:

The investigators linked ambient air pollution data from 151 U.S. metropolitan areas in 1980 with individual risk factor on 552,138 adults who resided in these areas when enrolled in a prospective study in 1982... Exposure to sulfate and fine particulate air pollution, which is primarily from fossil fuel combustion, was estimated from national data bases. Multivariate analysis controlled for smoking, education, and other risk factors. Increased mortality with increasing particulate air pollution was observed. Risk ratios of all-cause mortality for the most polluted areas compared with the least polluted equaled 1.15 and 1.17 when using sulfate and fine particulate measures respectively. Increased particulate air pollution was associated increased cardiopulmonary and lung cancer mortality but not with mortality due to other causes. Increased mortality is associated with sulfate and fine particulate air pollution at levels commonly found in U.S. cities. The increase in risk is not attributable to tobacco smoking...

Am J Respir Crit Care Med. 1995 Mar;151(3 Pt 1):669-74.

Particulate air pollution as a predictor of mortality in a prospective study of U.S. adults.

Pope CA 3rd, Thun MJ, Namboodiri MM, Dockery DW, Evans JS, Speizer FE, Heath CW Jr.Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts.

Sunday, April 10, 2005

Particle Studies in Community Settings - A Tree that Fell in the Occupational Health Forest, but Made No Noise

BrooklynDodger was conversating [a current expression in certain in certain inner city schools] with a colleague on particular workplace situation, when the fine particle question arose. Although the Dodger has blogged on this issue repeatedly, the Dodger felt that a series of posts on the evolution of this issue might prove helpful to reframing occupational health perceptions of a reference dose to particles with no other toxicity.

The big tree in this forest is the Harvard Six-Cities study.

The Dodger's extract from the abstract:

Survival analysis was conducted with data from a 14-to-16-year mortality follow-up of 8111 adults in six U.S. cities... After adjusting for smoking and other risk factors, we observed statistically significant and robust associations between air pollution and mortality. The adjusted mortality-rate ratio for the most polluted of the cities as compared with the least polluted was 1.26 ... Air pollution was positively associated with death from lung cancer and cardiopulmonary disease but not with death from other causes considered together... Mortality was most strongly associated with air pollution with fine particulates, including sulfates.

The full text of this seminal paper is available through medline for free, the Dodger invites readers to get it themselves. Obviously this was the bomb, combining Harvard and the New England Journal. It provoked political and scientific events to be described in later posts.

Important to note is the date of publication: more than a decade ago.

Also important to note, found only by reading the paper, is that these 6 cities were largely in compliance with the EPA then and now NAAQS for particulate. Exposure-response within this group of city provides clear evidence for hazard identification, and this is the only observation noted in the abstract. The exposure data in the study, however, provides an anchor for an exposure-response assessment for risk. BrooklynDodger opines that an acceptable exposure limit should be some factor below a no-effect level, which could be derived from these data.

If the Dodger were reviewing this paper, the Dodger would have asked the authors to include a sentence on the range of exposures in the abstract.


N Engl J Med. 1993 Dec 9;329(24):1753-9.

Comment in:
N Engl J Med. 1993 Dec 9;329(24):1807-8.
N Engl J Med. 1994 Apr 28;330(17):1237-8.
N Engl J Med. 2004 Jan 8;350(2):198-9.

An association between air pollution and mortality in six U.S. cities.

Dockery DW, Pope CA 3rd, Xu X, Spengler JD, Ware JH, Fay ME, Ferris BG Jr, Speizer FE.Environmental Epidemiology Program, Harvard School of Public Health, Boston, MA 02115.

Tuesday, April 05, 2005

Vitamin D and Calcium associated with increased colon cancer - another poorly edited abstract

A diet and cancer idea of which BrooklynDodger was unaware is that calcium and vitamin D prevent [or in epidemiologese, are negatively associated with the risk of] colon cancer. The publication abstracted below mines a mother lode of health data, the Women’s Health Study.

Paraphrased abstract:

The WHS in 1993 enrolled 39,876 women aged 45 or more and free of cardiovascular disease and cancer. This study reports on colon cancer observed over an average follow-up of 10 years. In that time, 0.55% of the women developed colorectal cancer [Dodger hasn’t read full text, assumes these are incident cases. Not very many cases, considering colon is in the top 3 cancer sites.] Based on diet questionnaires, a 20% increase in colon cancer, comparing highest quintile for calcium to the lowest, and a 34% increase for colon cancer for vitamin D intake were not significant. The investigators concluded the “Data provide little support for an association of calcium and vitamin D intake with colorectal cancer risk.”

Both the reviewers and the editor get demerits for a confusing and misleading abstract.

BrooklynDodger confesses that at first reading, the Dodger thought the authors were saying there was an improvement in experience that didn’t achieve significance. The Dodger was forced to go to the full text, to confirm that rates were higher in the expected protected group. The increased risk associated with Vitamin D was marginally significant – p <>

American Journal of Epidemiology 2005 161(8):755-764

Intakes of Calcium and Vitamin D and Risk of Colorectal Cancer in Women

Jennifer Lin1, Shumin M. Zhang1,2, Nancy R. Cook1,2, JoAnn E. Manson1,2,3, I-Min Lee1,2 and Julie E. Buring1,2,4 1 Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA2 Department of Epidemiology, Harvard School of Public Health, Boston, MA3 Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA4 Department of Ambulatory Care and Prevention, Harvard Medical School, Boston, MA

Correspondence to Dr. Jennifer Lin, Division of Preventive Medicine, Brigham and Women's Hospital, Harvard Medical School, 900 Commonwealth Avenue East, Boston, MA 02215 (e-mail: jhlin@rics.bwh.harvard.edu

Sunday, April 03, 2005

Particles Absorbed Through the Lung Cause Blood Clotting

Now that it's been established that increases in particulate air pollution are associated with [BrooklynDodger vacillated on whether to say "causes" or to back off to epidemiologese, and decided for today to go with the fuzzier scientific diction] increases in cardiovascular morbidity and mortality at the community level, laboratory studies are attempting to explain this observation.

The notable finding is that fine and ultrafine particles penetrate the lung into systemic circulation. This causes a profound shift in local concentration. Consider 70 micrograms of a substance dissolved into a 70 kg human body: concentration at the cellular level is 1 picogram per liter of body. [BrooklynDodger invites fact checking on this math; the Dodger picked 70 to avoid finding a calculator] As particles, the concentration at the particle surface approaches 1 kilogram per liter in contact with the biological material. That's a major change in physiology, especially for cascading effects like cancer, where a single cell can start a clone which grows to any size, or immunological effects.

This abstract, in paraphrase, notes:

Recently, we have demonstrated that ultrafine particles are able to translocate from the lung into the systemic circulation in hamsters and humans. We evaluated the acute effect (1 h) of diesel exhaust particles (DEP) in a hamster model of peripheral clotting induced by injury to blood vessel membranes. Intratracheal doses of 5-500 microg of DEP per animal induced inflammation with elevation of immune cells, total proteins and histamine in lung washing. DEP enhanced experimental arterial and venous platelet rich-thrombus formation in vivo. Blood samples taken from hamsters 30 and 60 min after instillation of DEP caused platelet activation. The direct addition of DEP to untreated hamster blood also caused platelet aggregation [pre clotting; the Dodger has to look at concentration]. These effects persisted up to 24 h after instillation.


Toxicol Lett. 2004 Apr 1;149(1-3):243-53.

Possible mechanisms of the cardiovascular effects of inhaled particles: systemic translocation and prothrombotic effects.

Nemmar A, Hoylaerts MF, Hoet PH, Nemery B.Laboratory of Pneumology, Unit of Lung Toxicology, K.U. Leuven, Herestraat, 49, Leuven 3000, Belgium. abderrahim.nemmar@med.kuleuben.ac.be

Saturday, April 02, 2005

Refinery Explosion

A March 23 explosion at the BP refinery in Texas City, TX killed 15 people, and injured about 70. It drove up the price of gasoline. So this tragedy raises the questions what could have prevented this event? and what was the role of OSHA? The standard which governs this situation is Process Safety Management of Highly Hazardous Chemicals. This rule is a legacy of Bhopal, implemented through Clean Air Act legislation which compelled OSHA to promulgate this rule.

Chemical process safety is best explained in an appendix to be found at


This rule was written by OSHA to have the minimum impact legally permissible given the authorizing legislation by excluding as many processes as possible, notably reactive chemicals and fuel tanks. BrooklynDodger will write more on this when the Dodger gets around to it.

What about the facility itself?

OSHA’s website publishes inspection data. http://www.osha.gov/oshstats/index.html

For reasons governed by the computer system, the Bp facility is invisible when searched under its name, but comes up in a search for SIC 2911. The facility was inspected based on a “referral” starting in March 2004. OSHA issued 14 serious citations for violations of the Process Safety Management standard (29 CFR 1910.119). This standard requires management to analyze processes for hazards which could cause explosions. Citations were issued in August 2004, with proposed penalties of $63,000. BP contested the citations. On a date unspecified, OSHA dropped 9 of the citations, and reduced the proposed penalty to $13,000. According to the OSHA website, this case remains open. The facility was again inspected following an accident, starting September 2, 2004. According to press reports, a pipe burst, killing two and injuring one. On February 25, 2005, OSHA issued one willful violation for lockout, with a fine of 70,000, and 7 serious violations totally 39500, for a total proposed penalty of $109,500. One of the serious citations was for process safety management violations. OSHA’s website says all penalties were contested March 21, 2005; some of these violations were claimed to be abated in March, 4 months after the incident. Press reports mentioned a death from a fall in May, 2004. No inspection appears in OSHA’s records related to that.


BP: Texas Plant 'Safe,' Death Toll at 15

March 24, 2005 2:31:00 PM ET TEXAS CITY, Texas (Reuters) -

BP Chief Executive John Browne said the company's Texas City, Texas, refinery ``a very safe plant'' on Thursday as the death toll in Wednesday's explosion there climbed to 15. It was the third fatal accident at the mammoth plant in the 12 months. A worker died in a fall last May, and two were killed and one injured in September when scalding hot water burst from a pipe.

A large explosion and fire also occurred last March 30, although no deaths or serious injuries were reported.

``It is a very safe plant,'' said Browne, who rushed to Texas following the blast. ``I think these events are unrelated, but there have been a few and we regret each one.'' …

In addition to the dead, 70 workers in the plant and 30 people in nearby areas were injured by the powerful explosion that shook buildings and broke windows several miles away.