Hiatus

First, I'm on the road. Second, blogspot is not letting me change the dates on posts, so that all my revisions are coming up with old dates.

Big Pharma Promotion

So let's take another whack at Big Pharma. The issue is drug promotion through physicians. Although these representatives are characterized as "saleswomen," the people they promote to are prescribers, not customers. And physician's offices tell you they meet with these reps because they provide free samples of medicines for patients that don't have drug coverage.

The Times below, even though the article is written by a woman, might be accused of a bit of sexism. There's little information on what these cheerleader women might have majored in. For example, Otwell, featured in the picture and a Survivor participant, is listed on the Survivor website as a "kinesiology" major [read phys. ed.] It's worth asking whether bachelor's degree people with no health education beyond should be promoting pharmaceuticals at all.

The Dodger has heard that orthopedic surgeons are frequently varsity athletes who went on. The story on orthopods is that they are "Strong as an Ox, and Twice as Smart."

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http://www.nytimes.com/2005/11/28/business/28cheer.html

Gimme an Rx! Cheerleaders Pep Up Drug Sales

By STEPHANIE SAUL

Published: November 28, 2005

As an ambitious college student, Cassie Napier had all the right moves - flips, tumbles, an ever-flashing America's sweetheart smile - to prepare for her job after graduation. She became a drug saleswoman.

Penny Otwell, a former cheerleader, is a drug sales representative.

Survivor: Penny Ramsey Otwell

Penny Otwell, a former cheerleader, is a drug sales representative.

Ms. Napier, 26, was a star cheerleader on the national-champion University of Kentucky squad, which has been a springboard for many careers in pharmaceutical sales. She now plies doctors' offices selling the antacid Prevacid for TAP Pharmaceutical Products.

Ms. Napier says the skills she honed performing for thousands of fans helped land her job. "I would think, essentially, that cheerleaders make good sales people," she said.

Anyone who has seen the parade of sales representatives through a doctor's waiting room has probably noticed that they are frequently female and invariably good looking. Less recognized is the fact that a good many are recruited from the cheerleading ranks.

Echoes of the Big Bang

[Richard Doll, Elisabeth Whelan and Julian Peto at an American Council for "Science" and "Health" (ACSH) function.]

Cosmologists see features of a singular event 15 billion years ago, or so, through radio astronomy. The Big Bang event created the universe and the natural laws according to which the universe functions. [You can buy this as an act of creation by the Deity, and a sign of the Deity's grandeur and power. However, "creationists" and "intelligent designers" believe the Deity returned, one or several times, to reshape the earth or life on earth.] About before the Big Bang we can know nothing.

For environmental health advocates interested in chemicals, there are multiple big bangs which shape our intellectual world. These were indeed intelligent design, since they are the works of historical figures. For cancer, these include Bernardino Ramazzini [who first noted hormonal cancers among celibate clerical women] and Percival Pott [who noted polynuclear aromatic chemical cancers among children employed as chimney sweeps.] The cigarette study by Doll and Hill is one of those events.

The study showed that inhaled particles caused lung cancer in people. The paper revealed the mother of all cohort mortality studies. The modern history began in 1954. The publication also spawned the strategy of scientific spin doctoring by industry, frequently noted in this blog as "money tox."

BrooklynDodger has previously noted that the laboratory toxicology of cigarette smoke is unknown to most in the chemical health field. Up until two years ago, the evidence for carcinogenicity of tobacco smoke from laboratory studies was only larynx cancer in hamsters, supported by equivocal studies in mice and rats, and implantation studies in a variety of species. Based on IARC criteria, this was sufficient evidence in laboratory studies. Absent human studies, cigarette smoke would be 2B, "possibly" carcinogenic. Based on NTP criteria, a positive association in one species is not enough for "reasonably anticipated" absent human data.

So, if we were FDA reviewing cigarettes in 1953, have the laboratory results, we would likely have approved cigarettes for commerce.

In later years, Doll came to stand for the idea that only cigarettes, and maybe asbestos, caused cancer in people. This is like the ripples in space time observed from the universe's Big Bang.


The BMJ reprint is available in full text
.>>>>

BMJ 2004;328:1529-1533 (26 June), doi:10.1136/bmj.328.7455.1529

Paper

The mortality of doctors in relation to their smoking habits: a preliminary report

(Reprinted from Br Med J 1954:ii;1451-5)

Richard Doll, M.D., M.R.C.P.¹, A. Bradford Hill, C.B.E., F.R.S.²

¹ Member of the Statistical Research Unit of the Medical Research Council, ² Professor of Medical Statistics, London School of Hygiene and Tropical Medicine; Honorary Director of the Statistical Research Unit of the Medical Research Council

The full text of this article is available in PDF format only.

Remember, Wood Dust is known to be a human carcinogen

[BrooklynDodger is having trouble with fonting in Firefox. Please excuse]

Wood Dust is one of the several human carcinogens completely ignored by OSHA. There isn't even a pre-1970 vintage PEL. The IARC summary will be posted separately. Natural doesn't mean non-toxic, or non-carcinogenic. Nasal cancer is most prominent among people; this suggests large particle exposure. Wood dust exposures are generated by low energy processes [compared to sawing concrete] without combustion, also a construct for large particles. [Nasal cancer and not other sites might be an artifact of the low population risk for nasal cancer, thus a smaller attributable risk could achieve statistical significance compared to lung. Do human lung tumors arise from the parenchema or from the bronchial tree?]

The investigators cite another paper for descriptions of where samples came from and how generated. The Dodger welcomes this least publishable unit approach which provides for another easy but useful post.

Bottom line: the IOM [open faced] sampler measured about 2x the mass of the 37 mm cassette, and the samples overall were 10 times normal workplace measurements.

"Table 1 Comparison of sampler means for all samples, samples not
containing ultra-large particles, and samples containing ultra-large
particles. Note that these values are about a factor of ten higher than
normal workplace measurements"

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Journal of Environmental Monitoring, 2004, 6(1), 18 - 22
DOI: 10.1039/b312883k

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Comparison of wood-dust aerosol size-distributions collected by air samplers

Martin Harper, Muhammad Zabed Akbar and Michael E. Andrew

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A method has been described previously for determining particle size distributions in the inhalable size range collected by personal samplers for wood dust. In this method, the particles collected by a sampler are removed, suspended, and re-deposited on a mixed cellulose-ester filter, and examined by optical microscopy to determine particle aerodynamic diameters. This method is particularly appropriate to wood-dust particles which are generally large and close to rectangular prisms in shape. The method was used to investigate the differences in total mass found previously in studies of side-by-side sample collection with different sampler types. Over 200 wood-dust samples were collected in three different wood-products industries, using the traditional 37 mm closed-face polystyrene/acrylonitrile cassette (CFC), the Institute of Occupational Medicine (IOM) inhalable sampler, and the Button sampler developed by the University of Cincinnati. Total mass concentration results from the samplers were found to be in approximately the same ratio as those from traditional long-term gravimetric samples, but about an order of magnitude higher. Investigation of the size distributions revealed several differences between the samplers. The wood dust particulate mass appears to be concentrated in the range 10–70 aerodynamic equivalent diameter (AED), but with a substantial mass contribution from particles larger than 100 µm AED in a significant number of samples. These ultra-large particles were found in 65% of the IOM samples, 42% of the CFC samples and 32% of the Button samples. Where present, particles of this size range dominated the total mass collected, contributing an average 53%(range 10–95%). However, significant differences were still found after removal of the ultra-large particles. In general, the IOM and CFC samplers appeared to operate in accordance with previous laboratory studies, such that they both collected similar quantities of particles at the smaller diameters, up to about 30–40 µm AED, after which the CFC collection efficiency was reduced dramatically compared to the IOM. The Button sampler collected significantly less than the IOM at particle sizes between 10.1 and 50 µm AED. The collection efficiency of the Button sampler was significantly different from that of the CFC for particle sizes between 10.1 and 40 µm AED, and the total mass concentration given by the Button sampler was significantly less than that given by the CFC, even in the absence of ultra-large particles. The results are consistent with some relevant laboratory studies.

Particle Size

The Dodger encountered this new journal while trolling medline. The author, Jim Vincent, is a solid citizen in the particle field.

The abstract is a model of conveying no information. The Dodger wonders, in addition, what's the difference between a "critical" review, a "systematic" review, and a just plain review. Is there a heirarchy? Below just plain reviews are there uncritical and unsystematic reviews?

Lurking behind the abstract in the full text is actually long and informative discussion of discussion of particle sizing advances since the Dodger went to industrial hygiene school.

There are at least two new things.

First is inhalable fraction, which includes particles larger than 10 microns [up to maybe 50]. In certain circumstances, like the WTC collapse, the large majority of the airborne mass is in this fraction which is excluded by the IH standard total particulate as measured by a closed face filter in a 37 mm cassette. Parallel with being aware that these particles exist, is recognition that reaction of the nasal surfaces can have systematic effects, such as observed among WTC recovery workers. Also, where the material may be absorbed, like lead, this near field divergence of actual mass from "total" mass may account for lack of correlation with body burden, and must be taken into account for quantitative risk assessment.

Second, we have the sub micron fraction, variously fine, ultrafine and nanoparticles. Most of the particle count in the fine [respirable, PM 2.5] is in the 1 micron range, arising from agglomeration of condensation processes. When you get below the 1 micron size, these particles are now known to penetrate the lung surfaces into systemic circulation.

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Critical Review

Journal of Environmental Monitoring, 2005, 7(11), 1037 - 1053
DOI: 10.1039/b509617k

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Health-related aerosol measurement: a review of existing sampling criteria and proposals for new ones

James H. Vincent

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Interest in particle size-selective sampling for aerosols in working and ambient living environments began in the early 1900s when it became apparent that the penetration into—and deposition in—the respiratory tract of aerosol-exposed humans of inhaled particles was dependent on particle size. Coarse particles tended to be filtered out during inhalation and in the upper parts of the respiratory tract, so only progressively smaller particles penetrated down to the deep regions of the lung. Over time, following experimental studies with breathing mannequins in wind tunnels and with human volunteer subjects in the laboratory, a clear picture has emerged of the physical, physiological and anatomical factors that control the extent to which particles may or may not reach certain parts of the respiratory tract. Such understanding has increasingly been the subject of discussions about aerosol standards, in particular the criteria by which exposure might be defined in relation to given classes of aerosol-related health effect—and in to turn aerosol monitoring. The ultimate goal has been to develop a set of criteria by which exposure standards are scientifically relevant to the health effects in question. This paper reviews the scientific basis for such criteria. It discusses the criteria that have already been widely discussed and so are either being applied or are on the threshold of practical application in standards. It also discusses how new advanced knowledge may allow us to extend the list of particle size-selective criteria to fractions that have not yet been widely discussed but which may be of importance in the future.

Periodic [Table] Musings

As the Dodger was having a dental implant screwed into the Dodger's head the other day, the thought came, why is titanium and titanium dioxide so inert, while iron and iron oxide so biologically active?

When the Dodger was in toxicology school, the story was that iron oxide was pretty benign. Siderosis was nothing to worry about. Has anyone ever looked at a case series of siderotics?

Think about a blast furnace. Fe2O3 + C = CO + Fe (metal). Substitute lung tissue for C. Iron oxide particles are burning up the lung tissue. "Oxidative stress" - a handwaving tox mechanism - metaphorically arises from the iron which is already there getting loose and donating oxygen to other structures.

Mechanism of Absorption of Ultrafine Particles

A second big bang for occupational and environmental health is the late 1990's observation of systemic health effects from insoluble inhaled particles. The Dodger reminds the reader these health effects include mortality from cardiac causes from exposures within the EPA community particle standard. These observations sparked laboratory toxicology, much the way the discovery of mortality associated with cigarette smoking sparked laboratory work. Unlike the cigarette toxicology, which only recently has replicated lung cancer mortality by inhalation, the particle project very quickly yielded results which provided biological plausibility to the epidemiological findings. Here, the investigators demonstrate the absorption of the archetypical non toxic non soluble titanium dioxide particles through the lumen and into cells. >>>>>>>>>>>>>>>>>>>>>>>>>> Environ Health Perspect. 2005 Nov;113(11):1555-60.

Ultrafine particles cross cellular membranes by nonphagocytic mechanisms in lungs and in cultured cells.

Geiser M, Rothen-Rutishauser B, Kapp N, Schurch S, Kreyling W, Schulz H, Semmler M, Im Hof V, Heyder J, Gehr P.

Institute for Anatomy, University of Bern, Bern, Switzerland. geiser@ana.unibe.ch

High concentrations of airborne particles have been associated with increased pulmonary and cardiovascular mortality, with indications of a specific toxicologic role for ultrafine particles (UFPs; particles < size="3">Within hours after the respiratory system is exposed to UFPs, the UFPs may appear in many compartments of the body, including the liver, heart, and nervous system. To date, the mechanisms by which UFPs penetrate boundary membranes and the distribution of UFPs within tissue compartments of their primary and secondary target organs are largely unknown. We combined different experimental approaches to study the distribution of UFPs in lungs and their uptake by cells. In the in vivo experiments, rats inhaled an ultrafine titanium dioxide aerosol of 22 nm count median diameter. The intrapulmonary distribution of particles was analyzed 1 hr or 24 hr after the end of exposure, using energy-filtering transmission electron microscopy for elemental microanalysis of individual particles. In an in vitro study, we exposed pulmonary macrophages and red blood cells to fluorescent polystyrene microspheres (1, 0.2, and 0.078 microm) and assessed particle uptake by confocal laser scanning microscopy. Inhaled ultrafine titanium dioxide particles were found on the luminal side of airways and alveoli, in all major lung tissue compartments and cells, and within capillaries. Particle uptake in vitro into cells did not occur by any of the expected endocytic processes, but rather by diffusion or adhesive interactions. Particles within cells are not membrane bound and hence have direct access to intracellular proteins, organelles, and DNA, which may greatly enhance their toxic potential.

Important Risk Assessment for Silica Shows Huge Risks at the Current OSHA PEL

Once in a while a paper appears in Regulatory Toxicology and Pharmacology which departs from its pervasive money tox outlook. This paper on silica, from California's EPA, aims to protect health. BrooklynDodger fears it leaves behind too much risk. The Dodger wonders whether this was introduced by regulators' limitations, was pressed on the authors by reviewers, or is a consequence of reviewers and editors asleep at the switch [latter unlikely.] Before launching into critique, the Dodger calls the readers' attention to the 3 microgram per cubic meter "limit" - compared to the 100 micrograms permitted by OSHA [inherited from the middle '60's], the 50 micrograms recommended by NIOSH [back in the early '70's]. Exposures in this range persist in the best controlled foundries, probably underground mines, sand pits, etc; the reference limit suggests hazards in agriculture and sweeping the streets. Also, the Dodger applauds California, and CalEPA, for continuing work to derive exposure limits and do risk assessements, now that OSHA and US EPA have stopped. "Reference" level is kind of weasel-word for health-based exposure not-quite limit. First, the endpoint is radiologically diagnosed silicosis, which is only a small part of the picture. The reference level in the title should be "silicosis" not silica. Silica exposure also causes reduced lung function [both restrictive and obstructive] and symptoms. At least twice as many additional workers are afflicted as have radiological silicosis. Second, radiological silicosis has an occult period - enough dose has been inhaled to cause effects that are not patent on x-ray. The occult period - might be called latency or lag - is 10 years or more. The Dodger didn't study the underlying studies to see how this was accounted for. By definition, 10 years of exposure includes 10 years of lag from first exposure, but the full bloom of the silica would only emerge after 20 years lag from the 10 years of exposure, or 30 years since hire. Third, mortality from lung cancer and mortality from non-malignant respiratory disease is equivalent in silica cohorts - about the same SMR and about the same number of observed deaths [Dodger will supply references in subsequent post]. However, none of the NMRD deaths on death certificate are silica. Lots are pneumonia. Hypothetically, silica potentiates other acute infectious lung disease just as it does tuberculosis. The risk assessment doesn't account for these non-pneumoconiotic endpoints. Fourth, the risk assessment doesn't take lung cancer into account. Fifth, the risk assessment doesn't justify the attack level for the benchmark dose. The reference level is the Benchmark Concentration Level 01 - a 1% attack rate statistically modeled from the data sets. Notably, because it's human data and chronic exposure data, CalEPA gives up those two uncertainty factors. CalEPA gives us a 3 fold uncertainty factor for intra species variability, which is definitely not risk averse. >>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>> Regul Toxicol Pharmacol. 2005 Sep 22; [Epub ahead of print]

Development of a chronic inhalation reference level for respirable crystalline silica.

Collins JF, Salmon AG, Brown JP, Marty MA, Alexeeff GV.

Air Toxicology and Epidemiology Branch, Office of Environmental Health Hazard Assessment, California Environmental Protection Agency, 1515 Clay Street, 16th Floor, Oakland, CA 94612, USA.

Chronic inhalation exposure of workers to crystalline silica can result in silicosis. The general public can also be exposed to lower levels of crystalline silica from quarries, sand blasting, and entrained fines particles from surface soil. We have derived an inhalation chronic reference exposure level for silica, a level below which no adverse effects due to prolonged exposure would be expected in the general public. Incidence of silicosis and silica exposure data from a cohort of 2235 white South African gold miners yielded a reference level of 3mug/m(3) for respirable silica (particle size as defined occupationally) using a benchmark concentration approach. Data from cohorts of American gold miners, Chinese tin miners, diatomaceous earth workers, and black South African gold miners yielded similar results with a range of 3-10mug/m(3). Strengths of the chronic reference exposure level include the availability of several large long-term studies of inhalation in workers at varying exposure concentrations, adequate histopathological and radiologic analysis, adequate follow-up of exposed workers, a dose-response effect in several studies, observation of a No Observed Adverse Effect Level in the key study, and the power of the key study to detect a small effect. Uncertainties include the general underestimation of silicosis by radiography alone and the uncertainties in exposure estimation.

Bacon II - Which Comes First, the Chicken or the Egg

[The other Francis Bacon, self portrait]

Back to "Truth arises more readily from error than confusion." This aphorism seems to contradict what Bacon stands for, which is inductive thinking from observation of the natural world. Historically Bacon might have been fighting scholastics who deduced natural phenomena from Aristotle's writings, rather than the world around them.

The Dodger is only marginally literate in philosophy of science; [for example, Popper gets a lot of play in the intelligent design debate, and in musings about Daubert, but the Dodger's never tasted his corn.] The Dodger, who claims to have practiced science at one point, thinks that a paradigm - theory - must exist for observations to even be observations. Kind of like framing. And people operating with different paradigms or frames may not even recognize the others' observations as observations.

Bench scientists collect particles of knowledge. Metaphorically, they aggregate observations. It takes the cement of a paradigm, theory, or frame, to create a concrete structure.

Regarding the chicken and egg, it's pretty simple. The first animal which laid a chicken's egg was not a chicken. And of course, the chicken is only the eggs way to make another egg, just like a building a car is just a dollar's way to make another dollar.

Bringing Home the Bacon

BrooklynDodger has quoted Bacon saying "Truth arises more readily from error than confusion." Aphoristically stated, a wrong paradigm can be tested and overturned by observations, but a collection of observations without a paradigm can't move forward. It's also an excuse to take a hard contrarian position against general doctrine. Kind of a wink to the audience... This is very important in occupational safety and health, where the received doctrine is mostly "blame the worker" and the audience is usually all management.

The Dodger thinks this quote was found in Kuhn, Structure of Scientific Revolutions. However, the Dodger has difficulty in finding the actual source of this quote. Bartlett's doesn't find it. So the Dodger went to google. Some internet sites aphorize without a reference to a source.

Some fiddling suggests the source is likely Novum Organum (1624). Figuring out which translation is which on the internet got discouraging. One document headed "New Organon" was searched with find/replace. Then the Dodger realized that whatever we are told Bacon said in English, he actually wrote it in Latin.

Anyway, the best the Dodger could do from an actual Bacon text was: "truth will sooner come out from error than from confusion."

Truck Sets Off Fire???

Many of us have seen Charlie Morecraft present on his tragic injury from a refinery explosion and fire. Charlie believes the ignition source at Exxon Bayway was a truck, his truck, left running.

This early account of the BP Texas City explosion also implicates an internal combustion engine.

Probably someone ought to test this theory, that is, figure out if the temperature of the outside of engine and exhaust surfaces can ignite vapors. If it can while running, how long does it take to cool down so it won't.


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http://www.chron.com/cs/CDA/ssistory.mpl/metropolitan/3110596

March 31, 2005, 11:27AM

Witnesses saw gas eruption before blast

Liquid and vapor may have been touched off by car engine or other ground source

By TOM FOWLER, DINA CAPPIELLO and KEVIN MORANCopyright 2005 Houston Chronicle

A geyser of liquid and vapor shot out of a 100-foot-tall ventilation tower at BP's Texas City refinery just seconds before an explosion last week that killed 15 people.

Silica and Renal Disease

Brooklyndodger recalls that going to IH school, we wondered why asbestos caused fibrosis and cancer, while silica only fibrosis. Since then, silica has become a known human carcinogen, based on mortality studies in people given biological plausibility by laboratory bioassays.

Now we wonder whether carbon black, carcinogenic in laboratory bioassays, is also carcinogenic in people.

Now comes an account of end stage renal disease and silicosis. The investigator notes a strong association - that is, a high relative risk. BrooklynDodger now needs to look for laboratory evidence to provide biological plausibility.

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Am J Ind Med. 2005 Jul;48(1):16-23.

One agent, many diseases: exposure-response data and comparative risks of different outcomes following silica exposure.
Steenland K.
Rollins School of Public Health, Emory University, 1518 Clifton Road, Atlanta, GA 30322, USA. nsteenl@sph.emory.edu

...The available exposure-response data for silica and silicosis, lung cancer, and renal disease are reviewed. We compare the corresponding excess risks (or absolute risks in the case of silicosis) of death or disease incidence by age 75 for these three diseases, subsequent to a lifetime (45 years) of exposure to silica at current US standard (0.1 mg/m(3) respirable crystalline silica).

...The absolute risk of silicosis, as defined by small opacities greater than or equal to ILO classification 1/1 on an X-ray, ranges from 47% to 77% in three cohort studies with adequate follow-up after employment. The absolute risk of death from silicosis is estimated at 1.9% (0.8%-2.9%), based on a pooled analysis of six cohort studies. The excess risk of lung cancer death, assuming US male background rates, is 1.7% (0.2%-3.6%), based on a pooled analysis of ten cohort studies. The excess risk of end-stage renal disease (assuming male background rates) is 5.1% (2.2%-7.3%), based on a single cohort. The excess risk of death from renal disease is estimated to be 1.8% (0.8%-9.7%), based on a pooled analysis of three cohorts. CONCLUSIONS: Keeping in mind that the usual OSHA acceptable excess risk of serious disease or death for workers is 0.1%, it is clear that the current standard is far from sufficiently protective of workers' health. Perhaps surprisingly, kidney disease emerges as perhaps a higher risk than either mortality from silicosis or lung cancer, although the data are based on fewer studies.

Carcinogens in the Neighborhood - Public Health Works, but does it work enough?

Probably the big 4 for scrutinized environmental chemical hazards are airborne particles, metals, POP's, and, mentioned here, volatile chlorinated hydrocarbons. Lately, particles have taken the lead for most evidence for adverse effects at prevailing levels. {BrooklynDodger also worries about volatile aliphatic hydrocarbons [gasolene, diesel fuel, etc], but laboratory evidence for carcinogenicity is now ignored by the EPA embrace of the Houdini risk assessment alpha-2 microglobulin hypothesis.} Small sources are an issue for population exposure. The sweet smell in the dry cleaner is perchlorotheylene [tetrachloroethylene]. Drycleaning consists of running your stuff through washing machines which use perc instead of water, and then dryers which aim to condense the perc so it can be reused. The gunk on your clothes are removed from the wash perc by running through column like a liquid chromatography column. The Dodger thinks the condensation is pretty efficient, so the sweet smell is fugitive emissions from wet clothing. New equipment is dry to dry, washing and drying in the same machine. Your neighborhood cleaner likely has a few 55 gallon drums of perc around too. Anyway, back to this post. Perc is carcinogenic in the 100 ppm inhalation range [see below]. Houdinists dispute the "relevance" of all these tumors to people. The rat leukemias are time dependent. The male rat kidney has generally been erased [not sure why these are called "rare" male rat kidney tumors] by alpha-2. Houdinists generally discount any mouse liver tumors, although hepatocellular carcinomas in female mice are harder to discount. Perc didn't cause lung tumors in the mice, which is a common outcome for volatile organics; mouse lung tumors are erasable by the mouse clara cell hypothesis. Perc was not genotoxic in multiple systems. [These assays don't discount gene silencing mechanisms.] The 100 ppm effect range is relatively more potent than other volatile organics. [The Dodger lazes today, and hasn't gone back to the pathology tables in the bioassay report to eyeball the NOAEL level; EPA IRIS should go 1000 fold below; for occupational the Dodger would use 100 fold below as a point of departure.] [Epidemiology in dry cleaners is mixed. NTP, quoting IARC, notes " Although these studies suggest a possible association between long-term occupational exposure to tetrachloroethylene and increased lymphatic malignancies and urogenital cancers, the evidence must be regarded as inconclusive because workers were exposed to petroleum solvents and other dry cleaning agents as well as tetrachloroethylene. When all studies are considered, there is evidence for consistent positive associations between tetrachloroethylene exposure and esophageal and cervical cancer and non-Hodgkin’s lymphoma. While these associations appear unlikely to be due to chance, confounding cannot be excluded; further, the total numbers in the cohort studies combined are relatively small (IARC 1995)." NTP further quotes " Typical tetrachloroethylene concentrations in workplace air at dry cleaning facilities were 350 to 700 mg/m3 (about 50 to 100 ppm) in the 1970s and 70 to 350 mg/m3 (about 10 to 50 ppm) in the 1980s (IARC 1995). The highest exposures occur when loading and unloading the dry cleaning machines;" The OSHA PEL for perc is 100 ppm. The ACGIH TLV for perc is 25 ppm. Obviously no margins here, for a carcinogen. Coming back to the environmental study. The conversion from ppm to mg/M3 for perc is 6.78. The 100 ug/M3 residential guideline cited below converts to 14 ppb. The 14 ppb ball parks to 10,000 fold below the 100 ppm effect level. The study below notes a mean exposure of 34 ug/M3, 17/65 apartments exceeding the limit. BrooklynDodger would have preferred the the authors, reviewers and editors have insisted on the median going into the abstract. The median, or geometric mean states the central tendency of distributions of environmental measurements better than the mean. The mean exposure of the population - the best measure of dose absorbed - is best estimated by calculation from the geometric mean and dispersion. This paper demonstrated a 10 fold reduction in exposure since NYC started to pay attention to this exposure. That's a validation of public health intervention. >>>>>>>>>>>>>>>>>>> Environmental Health Perspectives Volume 113, Number 10, October 2005

Tetrachloroethylene (PCE, Perc) Levels in Residential Dry Cleaner Buildings in Diverse Communities in New York City Michael J. McDermott,1 Kimberly A. Mazor,1 Stephen J. Shost,1 Rajinder S. Narang,2 Kenneth M. Aldous,2 and Jan E. Storm1 1Center for Environmental Health, New York State Department of Health, Troy, New York, USA; 2Wadsworth Center for Laboratories and Research, New York State Department of Health, Albany, New York, USA Abstract Fugitive tetrachloroethylene (PCE, perc) emissions from dry cleaners operating in apartment buildings can contaminate residential indoor air. In 1997, New York State and New York City adopted regulations to reduce and contain perc emissions from dry cleaners located in residential and other buildings. As part of a New York State Department of Health (NYSDOH) study, indoor air perc levels were determined in 65 apartments located in 24 buildings in New York City where dry cleaners used perc on site. Sampling occurred during 2001-2003, and sampled buildings were dispersed across minority and nonminority as well as low-income and higher income neighborhoods. For the entire study area, the mean apartment perc level was 34 µg/m3, 10-fold lower than mean apartment levels of 340-360 µg/m3 documented before 1997. The maximum detected perc level was 5,000 µg/m3, 5-fold lower than the maximum of 25,000 µg/m3 documented before 1997. Despite these accomplishments, perc levels in 17 sampled apartments still exceeded the NYSDOH residential air guideline of 100 µg/m3, and perc levels in 4 sampled apartments exceeded 1,000 µg/m3. Moreover, mean indoor air perc levels in minority neighborhoods (75 µg/m3) were four times higher than in nonminority households (19 µg/m3) and were > 10 times higher in low-income neighborhoods (256 µg/m3) than in higher income neighborhoods (23 µg/m3). Logistic regression suitable for clustered data (apartments within buildings) indicated that perc levels on floors 1-4 were significantly more likely to exceed 100 µg/m3 in buildings located in minority neighborhoods (odds ratio = 6.7; 95% confidence interval, 1.5-30.5) than in nonminority neighborhoods. Factors that may be contributing to the elevated perc levels detected, especially in minority and low-income neighborhoods, are being explored.Environ Health Perspect 113: 1336-1343 (2005). >>>>>>>>>>>>>>>>>>>>>>>> Toxicology and carcinogenesis studies of tetrachloroethylene (perchloroerhylene) in F344/N rats and B6C3F1 mice (inhalation studies) Authors: NTP Working Group National Toxicology Program Technical Report Series Vol:311 (1986) 197 p Toxicology and carcinogenesis studies of tetrachloroethylene (99% pure) were conducted by inhalation exposure of groups of 50 male and 50 female F344/N rats and B6C3F1 mice 6 hours per day, 5 days per week, for 103 weeks. The exposure concentrations used (0, 200, or 400 ppm for rats and 0, 100, or 200 ppm for mice) were selected on the basis of results from 13-week inhalation studies... Tetrachloroethylene was not mutagenic in salmonella typhimurium strains TA98, TA100, TA1535, or TA1537 in the presence or absence of male Syrian hamster or male Sprague-Dawley rat liver S9. Tetrachloroethylene was not mutagenic in L5178Y/TK mouse lymphoma cells with or without metabolic activation and did not induce sex-linked recessive lethal mutations in drosophila melanogaster. Tetrachloroethylene did not induce sister-chromatid exchanges or chromosomal aberrations in Chinese hamster ovary cells in the presence or absence of metabolic activation; Under the conditions of these 2-year inhalation studies, there was clear evidence of carcinogenicity of tetrachloroethylene for male F344/N rats as shown by an increased incidence of mononuclear cell leukemia and uncommon renal tubular cell neoplasms. There was some evidence of carcinogenicity of tetrachloroethylene for female F344/N rats as shown by increased incidences of mononuclear cell leukemia. There was clear evidence of carcinogenicity for B6C3F1 mice as shown by increased incidences of both hepatocellular adenomas and carcinomas in males and of hepatocellular carcinomas in female

PBB Ground Still Worth Zero

A blast from the past resurfaced in the Detroit News. PBB in Michigan. This goes to some musings about persistent organic pollutants. POP's, and the regulations controlling them, are front in the war over environmental protection.

POP's include PBB [mentioned here] but more broadly PCB's, dioxin, organochlorine pesticides. Risk assessment debates center on whether there are directly observable health effects in people, arising from exposures and body burdens which exist, or whether public health measures must be taken based on extrapolation from laboratory data in animals.

The history is from the Dodger's age addled memory. In 1973, polybrominated biphenyl (PBB) was added to cattle feed sold in Michigan, and apparently only in Michigan. Cows got sick, some died. Some of the dead cows were made into cattle feed and fed to other cows. Herds were culled, dead cows buried in land fills and through 1975 Michigan super markets would advertise "No Michigan Meat Sold Here."

PBB extrapolations include some directly observable health effects from animals, in this case, cows.

Laboratory studies established high dose toxicity; lab studies generally only can measure toxicity in the high dose range, because of small experimental group sizes, and also because rates of the health effect in control groups establish a floor below which health effects can't be seen. For PBB, carcinogenicity and liver toxicity presented from dietary exposures in the 3-30 parts per million range [ppm].

The Dodger got tired before finding a correlation of dietary levels to body burdens as measured by serum PBB concentrations. Serum PBB's in these studied women were in the range of 1-5 pbb [parts per billion.]

These studies individual fall in the realm of providing "some" evidence for health effects of PBB among exposured Michigan women. The menstrual study might be called "equivocal."

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http://www.detnews.com/2005/metro/0511/08/A01-375628.htm

Toxic town
Danger still stalks the families of tiny Michigan community
By Brad Heath / The Detroit News

It's site of PBB accident

The Velsicol Chemical plant closed in 1978.

But the real turning point came five years earlier, when workers there mistook bags of the flame-retardant PBB for animal nutrients. The chemical, believed to cause cancer, was mixed into livestock feed and distributed to farms around the state. Thousands of cows and more than a million chickens had to be slaughtered.

Velsicol never recovered. When the plant shut down, the company dug a hole in the ground and unceremoniously bulldozed the remains of their operation into it. Four years later, the company signed an agreement with the federal government requiring it to cover the dump with a layer of clay and surround it with an underground wall to keep the chemicals there from leaking out. In return, the government promised Velsicol Chemical, which took over the plant in the 1960s, it wouldn't have to pay for future cleanups.

The wall didn't work.

...
Environ Health. 2005 Aug 9;4:15.

Menstrual function among women exposed to polybrominated biphenyls: a follow-up prevalence study.

Davis SI, Blanck HM, Hertzberg VS, Tolbert PE, Rubin C, Cameron LL, Henderson AK, Marcus M.

Department of Epidemiology, Rollins School of Public Health, Emory University, 1518 Clifton Road, Alanta, GA 30322, USA. sidavis@cdc.gov

BACKGROUND: Alteration in menstrual cycle function is suggested among rhesus monkeys and humans exposed to polybrominated biphenyls (PBBs) and structurally similar polychlorinated biphenyls (PCBs). The feedback system for menstrual cycle function potentially allows multiple pathways for disruption directly through the hypothalamic-pituitary-ovarian axis and indirectly through alternative neuroendocrine axes. METHODS: The Michigan Female Health Study was conducted during 1997-1998 among women in a cohort exposed to PBBs in 1973. This study included 337 women with self-reported menstrual cycles of 20-35 days (age range: 24-56 years). Current PBB levels were estimated by exponential decay modeling of serum PBB levels collected from 1976-1987 during enrollment in the Michigan PBB cohort. Linear regression models for menstrual cycle length and the logarithm of bleed length used estimated current PBB exposure or enrollment PBB exposure categorized in tertiles, and for the upper decile. All models were adjusted for serum PCB levels, age, body mass index, history of at least 10% weight loss in the past year, physical activity, smoking, education, and household income. RESULTS: Higher levels of physical activity were associated with shorter bleed length, and increasing age was associated with shorter cycle length. Although no overall association was found between PBB exposure and menstrual cycle characteristics, a significant interaction between PBB exposures with past year weight loss was found. Longer bleed length and shorter cycle length were associated with higher PBB exposure among women with past year weight loss. CONCLUSION: This study suggests that PBB exposure may impact ovarian function as indicated by menstrual cycle length and bleed length. However, these associations were found among the small number of women with recent weight loss suggesting either a chance finding or that mobilization of PBBs from lipid stores may be important. These results should be replicated with larger numbers of women exposed to similar lipophilic compounds.

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Epidemiology. 2002 Mar;13(2):205-10.


Growth in girls exposed in utero and postnatally to polybrominated biphenyls and polychlorinated biphenyls.

Blanck HM, Marcus M, Rubin C, Tolbert PE, Hertzberg VS, Henderson AK, Zhang RH.

Biological and Biomedical Sciences Division, Rollins School of Public Health, Emory University, Atlanta GA 30322, USA.BACKGROUND: Accidental contamination with polybrominated biphenyls (PBBs) of the Michigan food supply in 1973 led to the exposure of more than 4000 individuals and to formation of the PBB cohort registry (1976-1979). At enrollment, measurements were taken of serum PBB and polychlorinated biphenyl (PCB), possible endocrine disrupting chemicals. METHODS: We examined the association of estimated PBB and PCB exposure during pregnancy with current height and weight in 308 daughters, 5-24 years of age (mean age 15.2 years), born to women in the cohort. We estimated prenatal PBB exposure using maternal enrollment serum PBB and a model of PBB elimination. Prenatal PCB exposure was estimated using maternal enrollment serum PCB because background-level exposure through diet was ongoing. Self-reported height and weight were obtained from a 1997-1998 health survey. RESULTS: We found no association between prenatal PBB exposure and either daughter's current height or daughter's weight adjusted for height; however, prenatal PCB exposure above 5 parts per billion was associated with reduced weight adjusted for height. Exposure through breastfeeding did not modify the association. CONCLUSIONS: Mothers with PCB levels above the median had daughters whose current weights were 11 pounds lower than that of the daughters whose mothers had levels below the median. This study provides evidence that prenatal exposure to PCBs may affect growth.

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Fundam Appl Toxicol. 1993 Nov;21(4):451-60.

Comparative carcinogenicity of polybrominated biphenyls with or without perinatal exposure in rats and mice.

Chhabra RS, Bucher JR, Haseman JK, Elwell MR, Kurtz PJ, Carlton BD.

National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709.

Chronic toxicity and carcinogenicity studies of a polybrominated biphenyl mixture (PBB) were conducted in F344/N rats and B6C3F1 mice of each sex. ...

During the perinatal period, rats were exposed to PBB at dose levels ranging from 1 to 10 ppm and adult exposure concentrations ranged from 3 to 30 ppm in the diet. In the mice, the dose levels ranged from 3 to 30 ppm in both perinatal and adult exposure portions of the chronic studies.

... Perinatal exposure alone (through dietary administration of 10 ppm PBB to the dams) had no effect on the incidences of neoplasms in female F344/N rats, but in male rats, perinatal exposure was associated with a marginally increased incidence of hepatocellular adenomas that may have been related to chemical administration. In male and female B6C3F1 mice, perinatal exposure to 30 ppm PBB resulted in significantly increased incidences of hepatocellular neoplasms. In adult-only dietary exposure studies, PBB was carcinogenic in male and female F344/N rats and male and female B6C3F1 mice based on increased incidences of hepatocellular neoplasms. ...
perinatal exposure enhanced the susceptibility of female rats receiving adult exposure of 10 or 30 ppm to the induction of liver neoplasms. For male and female rats, a combined analysis of the incidences of leukemia in the adult-only, perinatal-only, and combined perinatal and adult exposure groups revealed an apparent association between increasing incidences of mononuclear cell leukemia and exposure to PBB

[BrooklynDodger warns the reader that mononuclear cell leukemia in the rat is best observed in bioassays using mortality adjusted statistics. Few, maybe no industry sponsored bioassays use mortality adjusted statistics. Additionally, some public health opponents advocated ignoring all liver tumors in rodents, others emphasize ignoring mouse liver tumors.]

Neurology in an aging population

BrooklynDodger, getting on in years, spends time day to day joking with colleagues about losing mental edge, forgetting stuff, etc. Whistling in the dark. Maybe this posting isn't funny, but the Dodger started it and doesn't have the energy to find another paper.

Parkinson's is of some current interest to OH practitioners because of the apparent association with welding, and possibly prevailing exposures to manganese.

Parkinson's would not appear to have any aspect of cognitive causality, or projection on cognitive function. Nevertheless, whatever is causing the peripheral signs may also be causing problems with central functioning.

Disappointing on reading the full text is absence of the diagnostic questions which define "Excessive Daytime Sleeping" in this very old group of men, who average 77+ years. Feeling sleepy most of the day was the most the investigators would give us. EDS was found in about 8% of this population; the EDS group was more depressed, napped longer (not significant) and got up more at night. Plausibly the underlying process leading to presentation of Parkinson's signs is also causing sleep disturbances? Or maybe depressive processes which cause sleep disturbances?

Parkinson's incidence observed was 0.2 per 100 person years, elevated 3 fold among persons with EDS at entry.

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NEUROLOGY 2005;65:1442-1446

Excessive daytime sleepiness and subsequent development of Parkinson disease

R. D. Abbott, PhD, G. W. Ross, MD, L. R. White, MD, C. M. Tanner, MD, PhD, K. H. Masaki, MD, J. S. Nelson, MD, J. D. Curb, MD and H. Petrovitch, MD

From the Division of Biostatistics and Epidemiology (Dr. Abbott), University of Virginia School of Medicine, Charlottesville, VA; the Pacific Health Research Institute (Drs. Abbott, Ross, White, Masaki, Nelson, Curb, and Petrovich), the Department of Veterans' Affairs (Drs. Ross, White, and Petrovich), the Honolulu-Asia Aging Study, Kuakini Medical Center (Drs. Abbott, Ross, White, Masaki, Curb, and Petrovich), the Department of Geriatric Medicine (Drs. Abbott, Ross, Masaki, Curb, and Petrovich), the Department of Medicine (Drs. Ross, Curb, and Petrovich), and the Department of Pathology (Dr. Nelson), John A. Burns School of Medicine, University of Hawaii, Honolulu, HI; and the Parkinson's Institute (Dr. Tanner), Sunnyvale, CA.

Objective: To determine if excessive daytime sleepiness (EDS) can predate future Parkinson disease (PD).

Methods: EDS was assessed in 3,078 men aged 71 to 93 years in the Honolulu-Asia Aging Study from 1991 to 1993. All were free of prevalent PD and dementia. Follow-up for incident PD was based on three repeat neurologic assessments from 1994 to 2001.

Results: During the course of follow-up, 43 men developed PD (19.9/10,000 person-years). After age adjustment, there was more than a threefold excess in the risk of PD in men with EDS vs men without EDS (55.3 vs 17.0/10,000 person-years; odds ratio [OR] = 3.3; 95% CI = 1.4 to 7.0; p = 0.004). Additional adjustment for insomnia, cognitive function, depressed mood, midlife cigarette smoking and coffee drinking, and other factors failed to alter the association between EDS and PD (OR = 2.8; 95% CI = 1.1 to 6.4; p = 0.014). Other sleep related features such as insomnia, daytime napping, early morning grogginess, and frequent nocturnal awakening showed little relation with the risk of PD.
Conclusions: Excessive daytime sleepiness may be associated with an increased risk of developing Parkinson disease.

Cell Phones v. Radios for Traffic Accidents

Traffic incidents majorly cause traumatic injuries death and disability. The NSC and NHTSA focus on guilty victim behavior - safety belts and drunk driving - rather than treating these risk behaviors as effect modifiers for endemic behaviors like speeding, running red lights, and endemic environmental risk factors such as two lane roads curving downhill at night in the rain.

Lately there's been a boom in attacking cell phone use rather than addressing the overall social and environmental hazards.

The paper below compares effect of the cell phone vs. using adjusting radios [entertainment systems]. It's Australian data, so culturally suspect. The investigators note:

In an analysis of crashes caused by distraction,
Stutts et al.
(2001) identified outside people, objects or
events as the source of
distraction in 30% of driver distraction
cases and adjusting the
radio/cassette as the source in 11.4% of
cases. These were the most
frequently cited categories. Mobile
phones were the source of the distraction
in 1.5% of cases.

This was an observational study comparing impact of cell phone use to radio adjustment on speed, deviations from speed limits, and response to hazards.

Results were generally the same, the following for distraction causing drivers to slow down:

Paired samples t-tests indicated that the entertainment system
distracter produced a significantly lower mean speed than both the
no distracter condition and the phone
distracter. As such, the entertainment system
was more distracting to participants than the telephone conversation.
The phone distracter and the no distracter conditions
were not significantly different from each other.

>>>>>>>>>>>>>>>>>

No one seriously thinks of removing radios from cars. Stopping cell phone use, or penalizing drivers who use cell phones may be more convenient, if not logical since the radio is the bigger problem. More importantly, neither addresses the more pervasive problems in the driving environment.

>>>>>>>>>>>>>>>>>>>>>>
Accident Analysis and Prevention 38 (2006) 185–191

Driver distraction: The effects of concurrent in-vehicle tasks, road
environment complexity and age on driving performance

Tim Horberry a, Janet Anderson a,1, Michael A. Regan a, Thomas J. Triggs a, John Brownb
a Accident Research Centre, Monash University, Australia
b National Roads and Motorists’ Association, Australia

Annals of Computer Generated Bibliography

So the Dodger clicked the related articles button on this ergonomics low back injury paper. Look what came up: schizophrenia and atopy. Whatever artificial logic medline followed, it wasn't intelligence.

Luckily, BrooklynDodger wasn't beefing up ProCite, or the Dodger might have dumped these into a bibliography.

By the way, it's worth reading the Lavender paper. Various back risk factor methods don't correlate well. In the Dodger's opinion, the reason is that these measures were developed in conjunction with very short retrospective injury windows, so they all allow too much risk. Second, these measures don't account for the back injury risk associated with prolonged standing.

>>>>>>>>>>>>>>>>>>
Starting point, ergonomics:

Lavender SA. Oleske DM. Nicholson L. Andersson GB. Hahn J.
Comparison of five methods used to determine low back disorder risk in a manufacturing environment. [Journal Article]

Spine. 24(14):1441-8, 1999 Jul 15.
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find similar to Comparison of five methods used to determine low back disorder risk in a manufacturing environment.
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1.
Keshavan MS. Stanley JA. Montrose DM. Minshew NJ. Pettegrew JW. Prefrontal membrane phospholipid metabolism of child and adolescent offspring at risk for schizophrenia or schizoaffective disorder: an in vivo 31P MRS study. [Journal Article] Molecular Psychiatry. 8(3):316-23, 251, 2003 Mar. UI: 12660804

2.
Filipiak B. Heinrich J. Schafer T. Ring J. Wichmann HE. Farming, rural lifestyle and atopy in adults from southern Germany--results from the MONICA/KORA study Augsburg. [Journal Article] Clinical & Experimental Allergy. 31(12):1829-38, 2001 Dec. UI: 11737033

Ultrafine [dare we say nano] particles in an industrial setting

Occupational Hazards isn't a peer reviewed journal, but it here reports some cutting edge research on particle exposure in the occuaptional environment, which in turn provides information for exposures at home.

Direct-fired gas heaters prove to be a major source of ultra fine particles.

The major finding was, regardless of mass "Number concentrations of ultrafine particles inside the facility ranged from 15 to 150 times greater than outside the facility and were highly dependent on season. "Even in the assembly area where number concentrations were lowest, ultrafine particles were on average 15 times greater inside the facility than outside, regardless of the season."

Maybe 50 years ago, particle counting, collected via impinger, was the way to assess particle exposure. Sizing was visual. Then, balances got better, and mass collected on a filter became the measure. Cyclones or impacters provided sizing. Personal, breathing zone samples became feasible.

Now there are instruments which give real time, size specific particle counts, although personal samples are not yet feasible.

Particle number is plausibly the best measure for contact effects in the respiratory system - the number of spots impacted or phagocytic cells affected.

So now we identify a new and major source of particles, direct fired gas heaters. It's time to bioassay these particles in the rat, along with the effluent from a natural gas powered internal combustion engine.

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http://www.occupationalhazards.com/articles/14139
Study: Gas-Burning Heaters Cause Ultrafine Particle Spike in Engine Plant - 10/10/2005

Research has shown that "hot" processes such as welding and high-speed machining can generate ultrafine particles (particles with a diameter less than 100 nanometers) that may be harmful to workers' health. But a new study of nanoparticle levels in an Indianapolis engine machining and assembly plant concludes that a major source of nanoparticle emissions was the exhaust from its gas-burning heating system.
…
Researchers involved in the study found the greatest ultrafine particle number concentrations in the block-head-rod area, and they believe that the majority of ultrafine particles generated in that area came from direct-fire, natural gas burners that heated the supply air.

Researchers observed a nearly 1,000-percent spike in number concentration of ultrafine particles in the supply air when the heating system was operating compared to when it was turned off…

...

Ultrafine Particles 'Prevalent' Throughout Facility
…

1. Repeat analysis showed that these ultrafine particles "persist in the workplace over long time periods."

…
Mass Concentration Not a Good Indicator of Number Concentration

1. …

Overall, the study concludes that mass concentration was not a good indicator of number concentration.
"Mass concentration was low (less than 0.2 mg per cubic meter) where direct-fire heaters produced the greatest number concentration (more than 1 million particles per cubic centimeter)," Peters says. "Consequently, to the extent that health effects are related to ultrafine number exposures, current mass-based regulations may not be sufficient to protect workers in these areas."

BP Texas City Before March 23

The record $21 millin OSHA fine was paid by BP for citations following a March 23 explosion at the BP refinery in Texas City, TX which killed 15 people, and injured about 70. There’s probably an inside story at OSHA. But before March there was a serious OSHA history.

OSHA’s website reveals the following.

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.


http://news.moneycentral.msn.com/breaking/breakingnewsarticle.asp?feed=OBR&Date=20050324&ID=4327330

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.



http://www.chron.com/cs/CDA/ssistory.mpl/metropolitan/3110596

March 31, 2005, 11:27AM
Witnesses saw gas eruption before blast
Liquid and vapor may have been touched off by car engine or other ground source
By TOM FOWLER, DINA CAPPIELLO and KEVIN MORANCopyright 2005 Houston Chronicle
A geyser of liquid and vapor shot out of a 100-foot-tall ventilation tower at BP's Texas City refinery just seconds before an explosion last week that killed 15 people.

Bird Flu and Occupational Respiratory Disease Outbreaks

BrooklynDodger's posts on popcorn workers lung illustrate a previously unknown hazard being noted from a statistically unusual cluster of illnesses. Unfortunately, the outbreak was not noticed for nearly a decade after the index case was observed.

The Dodger bashes public health authorities for their "don't ask, don't tell, don't persue" mind set, particularly in relation to legionaire's disease.

An argument against a sentinel event system for respiratory disease is that a flu outbreak may be mistaken for a workplace problem. [Actually, if you work with chickens, the two might be the same.]

Effect Measure posts a benign explanation for the reticence of public health authorities. In 1976, public health authorities pulled the trigger on the pig flu. That was a time when Republicans would try to do something for public health, launching a immunization campaign against a real illness [not like smallpox]. But the pig flu never showed, and possible adverse reactions poisoned the well for the vaccination far into the future.

For public health officials, it's much worse for your career to pull the trigger on a response to a threat which never really presents, than it is to stand by and let it happen.

Based on CDC data, 2/1000 workers in hospital for respiratory diagnosis in a month, or 3/1000 on sick leave, is unusual and should trigger a response.

Popcorn Workers Lung (III) - Toxicology - Don't Ask, Don't Tell, Don't Pursue

Laboratory toxicology is a special NIOSH asset. As the endemic of popcorn workers lung was identified, environmental sampling identified diacetyl [2,3-butanedione] as the most prominent exposure. The peak exposure ranged to 100 ppm, the high exposure grouped medianed about 20 ppm, the largest exposed group medianed in the single digits.

Toxlining diacetyl revealed virtually nothing before 2002; a few papers on diacetyloxime. Toxlining diacetyl still reveals nothing beyond this one day exposure study in rats. Diacetyl is used in products other than popcorn. The Dodger thinks the butter smell of microwave popcorn is diacetyl, as well as the aroma of "I can't believe it's not butter." Human exposure is widespread. Yet the published literature contains no 2 week, 13 week or chronic bioassay of this material.

Wouldn't it be nice to know something about lower dose toxicity, or even a NOEL for a single 6 hour exposure?

Does the 1,2-dione structure have some specific biological activity leading to tissue damage? Is it binding to the respriatory epithelium?

Inquiring minds want to know. Inquiring minds would also be interested in whether FDA is dead, comatose, anethatized or just asleep at the switch.



>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
Toxicol Appl Pharmacol. 2002 Dec 1;185(2):128-35.

Necrosis of nasal and airway epithelium in rats inhaling vapors of artificial butter flavoring.

Hubbs AF, Battelli LA, Goldsmith WT, Porter DW, Frazer D, Friend S, Schwegler-Berry D, Mercer RR, Reynolds JS, Grote A, Castranova V, Kullman G, Fedan JS, Dowdy J, Jones WG. Health Effects Laboratory Division, National Institute for Occupational Safety and Health1, Centers for Disease Control and Prevention, 1095 Willowdale Road, Morgantown, West Virginia 26505, USA.

... Rats were exposed to vapors liberated from heated butter flavoring. Rats were exposed for 6 h by inhalation and were necropsied 1 day after exposure. The exposure was found by GC-MS analysis to be a complex mixture of various organic gases with the major peaks consisting of diacetyl (2,3-butanedione), acetic acid, acetoin (3-hydroxy-2-butanone), butyric acid, acetoin dimers, 2-nonanone, and delta-alkyl lactones. Diacetyl was used as a marker of exposure concentration. In the lung, butter flavoring vapors containing 285-371 ppm diacetyl caused multifocal, necrotizing bronchitis, which was most consistently present in the mainstem bronchus. Alveoli were unaffected. Butter flavoring vapors containing 203-371 ppm diacetyl caused necrosuppurative rhinitis, which affected all four levels of the nose. Within the posterior two nasal levels (T3 and T4), necrosis and inflammation was principally localized to the nasopharyngeal duct. Control rats were unaffected. Therefore, concentrations of butter flavoring vapors that can occur during the manufacture of foods are associated with epithelial injury in the nasal passages and pulmonary airways of rats.

Surgical strike from NSC, CDC to WHO

Surgical strike from NSC: Has CDC infected WHO?

From the NSC e-news letter comes the mis-information for workers exposed to chickens quoted below.

[Remember that joke with the punchline, “Chickens…ick!]

So the NSC parrot WHO who parrot CDC on “surgical masks.” Our US formulation “NIOSH approved N95 filtering facepiece respirator following annual fit tests” is maybe not recognized in an international context, but there has to be some formulation about protecting workers.

There’s literature suggesting that a surgical mask is more comfortable than an N95 [not clear if that’s for an N95 with an exhalation valve]. So if the surgical mask is to protect a patient from a health care worker’s aerosol exhalations, and you wouldn’t want an exhalation valve in that application, maybe it’s ok. Is there any science to back that up?

But obviously, the workers aren’t wearing these masks to protect the chickens. OH professionals don’t sufficiently credit the value of keeping mist and dust and big chunks of feathers and excrement from settling in and on the nose and mouth.

BrooklynDodger wonders, is there a literature on chicken workers’ allergy or any special syndrome demonstrating reaction to the organic dust associated with chickens? There’s plenty on laboratory workers exposed to rat dander, but those folks are sitting in a university setting waiting to be studied. There’s stuff on swine confinement workers [what’s the provenance of that, North Carolina, near UNC SPH, or some Scandinavian deal, Danish hams?] There’s Pigeon Breeders Disease [hypersensitivity pneumonitis, probably came to light in England or somewhere there are urban pigeon racers]

>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
International news
WHO: Protective clothing a must for poultry workers
Poultry workers, cullers and veterinarians should wear special clothing and take antiviral drugs to protect them from bird flu, according to the Geneva-based World Health Organization. WHO recommends workers wear coveralls, rubber gloves, surgical masks, goggles and rubber boots

Popcorn Worker's Lung (II) - Emergence of the Endemic

BrooklynDodger revealed his IH roots by starting the popcorn workers thread with exposure levels. The Dodger sympathized with the NIOSH team, parsing a pattern of devastating illness in relation to a chemical previously thought benign [diacetyl, or 2,3-butanedione].

The case study of interest would be the emergence of this situation on the ground from the perspective of the health care and public health practitioners. The USA Today article mostly tells the story from a victims perspective.

The quote immediately below is from the MMWR report, which appeared roughly simultaneously with the NEJM paper [same year being simultaneous]. It emerges that there were 8 victims of a very rare and severe condition in 8 years in a small town in Missouri. Who put this together, how, and why did it take that long?

The outbreak is maybe epidemic compared to the general population, but it was an endemic problem in the factory.

The next quote is from the on-the-ground NIOSH investigation. Typical of illness triggered HHE's, the investigators only accessed [had access to?] the current workers. The index cases, and possible additional cases who terminated [were terminated from?] employment for health reasons, are not in the survivor cohort. This practice is an endemic problem.

Therefore, the prevalence rates quoted in the abstract are prevalence among survivors and therefore do not reflect the full force of the toxic agent.

Finally comes the question of active case finding in the remaining facilities, and active measurement of the diacetyl and other exposures. Happening or not?

And even more finally, what's the diacetyl exposure level for consumers of products with artificial butter flavor. Are they still using diacetyl?

>>>>>>>>>>>>>>>>>>>>>>>>
http://www.usatoday.com/money/general/2002/06/20/popcorn-factory.htm

http://www.thoracic.org/assemblies/eoh/cases/feb03.asp http://jama.ama-

assn.org/cgi/content/extract/287/22/2939 MMWR. 2002;51:345-347

In May 2000, an occupational medicine physician contacted the Missouri Department of Health and Senior Services (MoDHSS) to report eight cases of fixed obstructive lung disease in former workers of a microwave popcorn factory. Four of the patients were on lung transplant lists. All eight had a respiratory illness resembling bronchiolitis obliterans with symptoms of cough and dyspnea on exertion, had worked at the same popcorn factory (factory A) at some time during 1992-2000, and had spirometric test results that were lower than normal for both FEV1 (forced expiratory volume in 1 second) and FEV1/FVC (forced vital capacity) ratio. Employment durations ranged from 8 months to 9 years. MoDHSS requested assistance from CDC's National Institute for Occupational Safety and Health in evaluating factory A for respiratory hazards to workers.

>>>>>>>>>>>>>>>>>>

Of the 116 participating employees who underwent spirometric testing, 31 had abnormal results on spirometry: 10 had low FVC values alone, 11 had airway obstruction alone, and another 10 had airway obstruction and low FVC values. The prevalence of airway obstruction increased with increasing cumulative exposure to diacetyl. The rates of airway obstruction, according to quartiles of increasing exposure, were 10.3 percent, 10.3 percent, 24.1 percent, and 27.6 percent (P for trend=0.03). The proportion of workers with abnormal results on spirometry (airway obstruction or a low FVC value) also increased with increasing cumulative exposure, to 13.8 percent, 24.1 percent, 31.0 percent, and 37.9 percent in successive quartiles (P for trend=0.02). Workers in each quartile of increasing cumulative exposure to diacetyl had decreasing average FEV1 values (Figure 2). The average FEV1 was 4.5 percent, 8.9 percent, and 12.5 percent lower than the predicted value in the second, third, and fourth quartiles of diacetyl exposure, respectively, than in the first quartile.

>>>>>>>>>>>>>>>>>>>>>>>>>>>
N Engl J Med. 2002 Aug 1;347(5):330-8.

Clinical bronchiolitis obliterans in workers at a microwave-popcorn plant.

Kreiss K, Gomaa A, Kullman G, Fedan K, Simoes EJ, Enright PL.

Division of Respiratory Disease Studies, National Institute for Occupational Safety and Health, Morgantown, WVa 26505, USA. kkreiss@cdc.gov

...In May 2000, eight persons who had formerly worked at a microwave-popcorn production plant were reported to have severe bronchiolitis obliterans. No recognized cause was identified in the plant. ... We evaluated the relation between exposures and health-related outcomes by analyzing the rates of symptoms and abnormalities according to current and cumulative exposure to diacetyl, the predominant ketone in artificial butter flavoring and in the air at the plant. ... Of the 135 current workers at the plant, 117 (87 percent) completed the questionnaire. These 117 workers had 2.6 times the expected rates of chronic cough and shortness of breath, according to comparisons with the national data, and twice the expected rates of physician-diagnosed asthma and chronic bronchitis. Overall, the workers had 3.3 times the expected rate of airway obstruction; those who had never smoked had 10.8 times the expected rate. Workers directly involved in the production of microwave popcorn had higher rates of shortness of breath on exertion and skin problems that had developed since they started work than workers in other parts of the plant. There was a strong relation between the quartile of estimated cumulative exposure to diacetyl and the frequency and extent of airway obstruction. ...

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From USA Today:

Below is a partial list of factories in the U.S. that reportedly produce microwave popcorn and other snack foods. This list is not meant to imply that any workers at these plants have been injured by exposure to artificial butter flavoring.

CaliforniaConagra Grocery Products, Irvine; Gaslamp Popcorn Company, San Diego ConnecticutLincoln Snacks Company, Stamford; Newman's Own, Westport FloridaBarnard Nut Company, Miami IllinoisCornfields, Gurnee; Gilster-Mary Lee Corp., Chester; Lee Gilster-Mary Corp., Momence; Tee Lee Popcorn, Shannon IndianaAmish Country Popcorn, Berne; Ellis Popcorn Co., West Terre Haute; Family Time Popcorn, Inc., Valparaiso; Gettelfinger Popcorn, Palmyra; Jones Popcorn, New Albany; Kirk's Popcorn Co., Topeka; Vogel Popcorn, Corydon; Weaver Popcorn Co., Markle, Crawfordsville, Huntingburg, Van Buren, Indianapolis & New Richmond; Yoder Popcorn Inc., Topeka IowaAmerican Pop Corn Co., Sioux City; Conagra Foods, Hamburg; Manson Industries, Manson; Noble Distributor, Sac City KentuckyEllis Popcorn Company, Murray MassachusettsNew England Pretzel & Popcorn, Lawrence MinnesotaConagra Foods, Minneapolis MissouriMary Lee Packaging Corp., Perryville NebraskaLincoln Snacks Company, Lincoln PennsylvaniaReist Popcorn Company, Mount Joy South CarolinaInternational Cup Corp., Bennettsville; Soller, Bennettsville