BP explosion and safety

BrooklynDodger notes that the three largest OSHA penalties assessed were 1.3 million against Union Carbide during the Reagan Administration, 7 million against USX during the Bush I administration, and now 21 million against BP during Bush II. The Dodger had noted the first incidents when Bush II was appointed, perhaps whistling in the dark that all was not lost in H&S after the disappointing Clinton years. The Dodger fears that corporate management heard the labor critique of the Bush II OSHA, and walked away from safety and health concerns, and hopes that management will now remember that lightning struck 3 times during conservative administrations, and could strike a 4th. Unlike the previous two cases, where OSHA settled out the citations for far less than the press release amounts, this pre-citation settlement is an agreed to penalty.

A month before the OSHA announcement, the Chemical Safety Board (CSB) issued an emergency statement:

http://www.csb.gov/news_releases/docs/BP

BrooklynDodger recommends that safety types take a look at the interim recommendations by the Chemical Safety Board to BP, following a series of incidents which befell the corporation after the March explosion.

The CSB BP recommendations include an external safety panel.

BrooklynDodger hopes that the CSB will also make recommendations for OSHA.

Association of Risk Factors for Breast Cancer with Types of Work

Another paper observes that physical activity at work protects women against breast cancer.  This implies a healthier worker effect for breast cancer among women whose work activities are in factories with notable chemical exposures.

It’s well established that women in “professional” jobs are at increased risk compared to those who are not.  Social class and education associate with other “lifestyle” issues like age at first childbirth, diet, time to exercise outside of work.  BrooklynDodger hopes for a quantitative measure of the metabolic activity of various kinds of work, and a distribution of this activity by occupational class.

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Kruk, J. and Aboul-Enein, H. Y.
Occupational physical activity and the risk of breast cancer.
Cancer Detect Prev. 2003; 27(3):187-92.

The association between occupational and the risk of breast cancer was analyzed using data from a case-control study of 257 women with breast cancer and 565 control women. After adjusted for potential confounders, women in sedentary occupations had a 29% higher risk, compared to those with the physically medium demanding jobs. For women at age > or =55 years higher occupational physical levels were associated with 53-60% reduction in the risk. There was a significant decreasing trend in the ORs from sedentary to medium work (P=0.001); while no association emerged in younger women.

Risk Factors for Breast Cancer - How to Keep them Straight?

Given the lack of cohorts of women with heavy occupational chemical exposures, environmental chemical causes of cancer among women are poorly identified. The majority of human carcinogens have first been observed in occupational settings. Which is not a deal for lung cancer, we expect the agents to be the same. But for female breast cancer we need data in females.

[Actually, the overwhelming risk factor for breast cancer is being female. Estrogen poisoning?]

The next issue is, what are the population risk factors for breast cancer, so as to look at modifiers of a chemical exposure effect in an occupational population? What is the appropriate healthy worker effect among women for female breast, ovarian and other cancers?

The most objective issue is physical activity. Physical activity is generally agreed to be protective, although the biological basis for this is speculative. Factory workers have way more physical demands than the general population, and this is likely more pronounced for woman than men. So factory women would be expected to have reduced breast cancer compared to the general population. This has been observed.

What about other risk factors? Early menarche [and late or no child birth] is a risk factor for breast cancer. Height is a risk factor for breast cancer. However, early menarche is a risk factor for not being tall. In this paper, as a population, in Europe, women as a population are getting taller in spite of having earlier menarche. Both height and menarche are plausibly products of improved nutrition.

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American Journal of Epidemiology 2005 162(7):623-632; doi:10.1093/aje/kwi260


Age at Menarche in Relation to Adult Height
The EPIC Study
N. C. Onland-Moret1, P. H. M. Peeters1, C. H. van Gils1, F. Clavel-Chapelon2, T. Key3, A. Tjønneland4, A. Trichopoulou5, R. Kaaks6, J. Manjer7, S. Panico8, D. Palli9, B. Tehard2, M. Stoikidou5, H. B. Bueno-De-Mesquita10, H. Boeing11, K. Overvad12, P. Lenner13, J. R. Quirós14, M. D. Chirlaque15, A. B. Miller16, K. T. Khaw17 and E. Riboli6
1 Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, the Netherlands2 E3N-EPIC Group, Institute Gustav Roussy, National Institute for Health and Medical Research (INSERM), Villejuif, France3 Cancer Research UK Epidemiology Unit, University of Oxford, Oxford, United Kingdom4 Institute of Cancer Epidemiology, Danish Cancer Society, Copenhagen, Denmark5 Department of Hygiene and Epidemiology, Medical School, University of Athens, Athens, Greece6 International Agency for Research on Cancer (IARC), Lyon, France7 Department of Community Medicine, Malmö University Hospital, Malmö, Sweden8 Dipartimento di Medicina Clinica e Sperimentale, Universita Federico II, Naples, Italy9 Molecular and Nutritional Epidemiology Unit, Centro per lo Studio e la Prevenzione Oncologica, Istituto Scientifico della Regione Toscana, Florence, Italy10 Centre for Nutrition and Health, National Institute for Public Health and Environment, Bilthoven, the Netherlands11 Department of Epidemiology, German Institute of Human Nutrition, Bergholz-Rehbruecke, Germany12 Department of Clinical Epidemiology, Aalborg Hospital, Aarhus University Hospital, Aalborg, Denmark13 Department of Oncology, Umeå University, Umeå, Sweden14 Public Health and Health Planning Directorate, Asturias, Spain15 Epidemiology Department, Regional Health Council, Murcia, Spain16 Division of Clinical Epidemiology, Deutsches Krebsforschungszentrum, Heidelberg, Germany17 Clinical Gerontology Unit, University of Cambridge, Cambridge, United Kingdom
Correspondence to N. C. Onland-Moret, Julius Center for General Practice and Patient Oriented Research, Room Str-6.119, University Medical Center Utrecht, P.O. Box 85500, 3508 GA Utrecht, the Netherlands (e-mail: N.C.Onland@jc.azu.nl (image placeholder).
In the last two centuries, age at menarche has decreased in several European populations, whereas adult height has increased. It is unclear whether these trends have ceased in recent years or how age at menarche and height are related in individuals. In this study, the authors first investigated trends in age at menarche and adult height among 286,205 women from nine European countries by computing the mean age at menarche and height in 5-year birth cohorts, adjusted for differences in socioeconomic status. Second, the relation between age at menarche and height was estimated by linear regression models, adjusted for age at enrollment between 1992 and 1998 and socioeconomic status. Mean age at menarche decreased by 44 days per 5-year birth cohort (ß = –0.12, standard error = 0.002), varying from 18 days in the United Kingdom to 58 days in Spain and Germany. Women grew 0.29 cm taller per 5-year birth cohort (standard error = 0.007), varying from 0.42 cm in Italy to 0.98 cm in Denmark. Furthermore, women grew approximately 0.31 cm taller when menarche occurred 1 year later (range by country: 0.13–0.50 cm). Based on time trends, more recent birth cohorts have their menarche earlier and grow taller. However, women with earlier menarche reach a shorter adult height compared with women who have menarche at a later age.

Fine Particles and Acute Inflammation Effects at 10 ug

BrooklynDodger fears prior posting of this clinical study of ultrafine particle effects. Nevertheless, it goes up again, and will likely appear yet another time when the technical report to the Health Effects Institute appears in a peer reviewed journal.

BrooklynDodger also neglected to return to the original to see where the investigators got the ultrafine particles or how they adjusted the concentration or followed agglomeration. Since these are 0.1 micron in diameter at less, they could also be called “nanoparticles,” a jazzier name. As carbon particles, these would formerly be thought inert.

Bottom line is that 10 ug/M3 for 2 hours is an effect level for various circulating cellular indications of inflammation. Some in asthmatics only, some in healthy volunteers as well.

BrooklynDodger notes that Gunter Oberdorster and the laboratory at the University of Rochester have emerged as major authorities on this subject.

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Res Rep Health Eff Inst. 2004 Dec;(126):1-47;
Effects of exposure to ultrafine carbon particles in healthy subjects and subjects with asthma.Frampton MW, Utell MJ, Zareba W, Oberdorster G, Cox C, Huang LS, Morrow PE, Lee FE, Chalupa D, Frasier LM, Speers DM, Stewart J.University of Rochester Medical Center, NY 14642-8692, USA. mark_frampton@urmc.rochester.eduUltrafine particles (UFP; less than 0.1 microm in aerodynamic diameter) may contribute to the health effects of particulate matter (PM) because of a higher predicted pulmonary deposition, greater potential to induce pulmonary inflammation, larger surface area, and enhanced oxidant capacity and the potential to cross the epithelium and enter the systemic circulation. Three clinical exposure studies: healthy subjects breathing filtered air and UFP (10 microg/m3) at rest; healthy subjects breathing air and UFP (10 and 25 microg/m3) with intermittent exercise; and subjects with mild asthma breathing air and UFP (10 microg/m3) with intermittent exercise. All exposures were for 2 hours. For healthy subjects, the fractional deposition of UFP at rest was 0.66 by particle number. Deposition further increased during exercise (0.83). Asthmatic subjects showed higher UFP deposition than did healthy subjects when breathing at rest (0.76 +/- 0.05). Breathing 25 microg/m3 UFP with exercise (UPDOSE) was associated with reductions in blood monocytes and activation of T lymphocytes in healthy females. In asthmatic subjects, breathing 10 microg/m3 UFP was associated with reduced numbers of blood eosinophils and CD4+ T lymphocytes. Monocyte expression of intercellular adhesion molecule-1 (ICAM-1) was reduced in a concentration-related manner (P = 0.001). In the UPASTHMA group, CD11b expression was reduced on monocytes and eosinophils, and ICAM-1 expression was reduced on polymorphonuclear leukocytes (PMNs). ECG analyses of UPDOSE subjects showed transient reductions in parasympathetic influence on heart rate variability and a reduced repolarization (QT) interval. In UPASTHMA subjects, ECG analyses showed decreased QT variability, but no effect on the QT interval. There were no significant effects in any of the studies on symptoms, pulmonary function, or markers of airway inflammation. The observed subtle changes in leukocyte subsets and adhesion molecule expression are consistent with effects on vascular endothelial function. We also found effects [in an adverse direction] on heart rate variability and on cardiac repolarization in healthy subjects.

Even a Houdini risk assessment finds risks in occupational environment - TCE

Even a Houdini risk assessment has a hard time making an occupational exposure risk disappear.  The OSHA PEL for TCE is 100 ppm, about 5,000 mg/M3.  
The authors, one from the Chemical Industry Institute of Toxicology, and the other from ENVIRON “Institute” approach the EPA risk assessment for TCE.  Without tracking down the full text and seeing the acknowledgements, BrooklynDodger wonders whether this is a grant from CIIT to Environ, sort of pro malo on CIIT’s part, or whether there was a specific sponsor.  The big money in TCE is drinking water disinfection products or groundwater contamination.  
The authors note that EPA’s quantitative risk assessment, based on mitogenicity [increased cell division] of TCE metabolites, finds a 1.5 per million cancer risk at 1 ug/M3 exposure. [If it’s all linear, that would say 1 mg/M3, or about 1/5 ppm would generate the canonical 1/1000 risk benchmark for OSHA carcinogens.]
The authors assert as true their preferred mechanism, and state:  “Based on consideration of the most plausible carcinogenic modes of action of TCE, a margin-of-exposure (MOE) approach would appear to be more appropriate. Applying an MOE of 1000, environmental exposures below 66 μg TCE per cubic meter in air…would be unlikely to present a carcinogenic risk to human health.”
Rounding, 66 ug/M3 is about 0.8 ppb in air.  Taking away the MOE, we get back to 1 ppm.  If 1000 fold below is “unlikely,” is 1 ppm “likely”?  Anyway, the number is still 100-fold below the PEL.
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Incidentally, the Dodger wondered what’s up with Ruston.  Ruston is east of Shreveport, the home of Louisiana Tech.  Prior to Environ, LT was on the map because of Terry Bradshaw:
When Bradshaw was a student at Louisiana Tech he joined the Tau Kappa Epsilon Fraternity. After graduating from Louisiana Tech, Bradshaw was the first player selected in the 1970 NFL draft. During his first several seasons, the 6'3" (190 cm), 215 lb. (97 kg) quarterback was erratic, and was ridiculed by the media for his rural roots and perceived lack of intelligence.
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Critical Reviews in Toxicology Volume 34, Issue 5 , 2004, Pages 385-445
Applying mode-of-action and pharmacokinetic considerations in contemporary cancer risk assessments: An example with trichloroethylene
Harvey J. Clewell1, and Melvin E. Andersen2 1ENVIRON Health Sciences Institute, Ruston, Louisiana, USA2CIIT Centers for Health Research, Research Triangle Park, North Carolina, USA Available online 23 September 2005. Abstract
The guidelines for carcinogen risk assessment recently proposed by the U.S. Environmental Protection Agency (U.S. EPA) provide an increased opportunity for the consideration of pharmacokinefic and mechanistic data in the risk assessment process. However, the greater flexibility of the new guidelines can also make their actual implementation for a particular chemical highly problematic. To illuminate the process of performing a cancer risk assessment under the new guidelines, the rationale for a state-of-the-science risk assessment for trichloroethylene (TCE) is presented. For TCE, there is evidence of increased cell proliferation due to receptor interaction or cytotoxicity in every instance in which tumors are observed, and most tumors represent an increase in the incidence of a commonly observed, species-specific lesion. A physiologically based pharmacokinetic (PBPK) model was applied to estimate target tissue doses for the three principal animal tumors associated with TCE exposure: liver, lung, and kidney. The lowest points of departure (lower bound estimates of the exposure associated with 10% tumor incidence) for lifetime human exposure to TCE were obtained for mouse liver tumors, assuming a mode of action primarily involving the mitogenicity of the metabolite trichloroacetic acid (TCA). The associated linear unit risk estimates for mouse liver tumors are 1.5 × 10−6 for lifetime exposure to 1 μg TCE per cubic meter in air and 0.4 × 10−6 for lifetime exposure to 1 μg TCE per liter in drinking water. However, these risk estimates ignore the evidence that the human is likely to be much less responsive than the mouse to the carcinogenic effects of TCA in the liver and that the carcinogenic effects of TCE are unlikely to occur at low environmental exposures. Based on consideration of the most plausible carcinogenic modes of action of TCE, a margin-of-exposure (MOE) approach would appear to be more appropriate. Applying an MOE of 1000, environmental exposures below 66 μg TCE per cubic meter in air and 265 μg TCE per liter in drinking water are considered unlikely to present a carcinogenic hazard to human health.
Keywords: Cancer risk assessment; Mode-of-action; Pharmacokinetics; Trichloroethylene (image placeholder)

Address correspondence to Harvey J. Clewell, ENVIRON Health Sciences Institute, Ruston, LA 71270, USA.

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Particle Toxicity in vitro

BrooklynDodger fears complexity in particle response will found a new line of Houdini risk assessments to avoid a single particle limit, either in the community or at work.  Appropriate recognition of varying responses of several cell types and several particle types would explain some contrasting whole animal people responses.  The Dodger fears slicing and dicing of response data to attempt multiple limits.

So here the investigators find 3 types of inflammatory cells in the airways: neutrophils (PMN), eosinophils and monocytes (Mo), and alveolar macrophages (AM).  They chose 6 types of particles:  transition metal-rich residual oil fly ashes (ROFAs), coal fly ashes, diesel, SiO2, TiO2 and fugitive dusts [which contained aluminum silicates].  The particles were of various sizes.  Different cells reacted differently to different particles of different size and source.  There’s at least an 18 cell matrix showing relative sensitivity of cell type vs. particle type.

The main message is that the so called inert material, titanium dioxide, reacted with all these cell types.  Diesel, theoretically a carbon particle coated with PAC’s [PAC’s not being acutely reactive?] also had effect.

The claims of those who believe no physiological basis for fine particle epidemiology are clearly weakened.

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 Toxicol In Vitro. 2002 Jun;16(3):209-18
Differential particulate air pollution induced oxidant stress in human granulocytes, monocytes and alveolar macrophages.Becker S, Soukup JM, Gallagher JE.US EPA, Office of Research and Development, National Health and Environmental Effects Research Laboratory, Research Triangle Park, NC 27711, USA. becker.susanne@epamail.epa.gov Individuals with pre-existing airways inflammation, such as chronic obstructive pulmonary disease (COPD), lung infection or asthma are likely most sensitive to particulate pollution. These diseases are characterized by a presence of inflammatory cells in the airways including neutrophils (PMN), eosinophils and monocytes (Mo), and increased numbers of alveolar macrophages (AM).  Particles including transition metal-rich residual oil fly ashes (ROFAs), coal fly ashes, diesel, SiO2, TiO2 and fugitive dusts were co-cultured with AM, Mo and PMN. A strong oxidant response of AM was restricted to oil fly ashes, while the PMN were most reactive to the dusts containing aluminium silicate. In general, the Mo response was less vigorous, but overlapped both AM- and PMN-stimulating dusts. The response of AM to SiO2 of various sizes and TiO2 in the fine size range obtained from different commercial sources, was highly variable, implying that composition rather than size was responsible for the oxidant response. These results suggest that oxidant activation by various sources of particulate matter is cell specific. Therefore, the inflamed lung is likely to be more susceptible to harm of ambient air particulates because of the oxidant stress posed by a broader range of particles.

Bogosity - Thy Name is Sociobiology

BrooklynDodger apologizes for being so late bringing this post to the blog, probably too late to get the orginal Times article without paying. As time has passed, the Dodger wonders the point of this blog, but there is too much work here to just blow it away.

This article on animal behavior had multiple echoes. It parallels the now routine article about what part of the brain lights up on MRI when the subject sees naked people, and whether straights and gays light up the same. [Whatever straights and gays are.]

The first question with this stuff is whether the outcome observations are any good. BrooklynDodger wonders whether vole behavior, the dances of the fruit flies, and the MRI's are all that easy to tell one from the other. Especially the vole behavior. Even in cages. What was their N? What was their inter-rater variability?

The second question is biological plausibility. Genes make proteins [actually, the gene makes an RNA and the RNA makes the proteins]; maybe they also make RNA's with regulatory functions and no proteins. The behavioral phenotype is obviously multi-genic; the phenotype likely can be turned off by a single allele - blind voles might be poor mates. [Maybe not the best example, if they are noctornal and do it by smell, but maybe it's a smell gene where the male vole can't tell females in the dark.]

A Gene for Romance? So It Seems (Ask the Vole)


By NICHOLAS WADE
Published: July 19, 2005
Biologists have been making considerable progress in identifying members of a special class of genes - those that shape an animal's behavior toward others of its species. These social behavior genes promise to yield deep insights into how brains are constructed for certain complex tasks.

Some 30 such genes have come to light so far, mostly in laboratory animals like roundworms, flies, mice and voles. Researchers often expect results from these creatures to apply fairly directly to people when the genes cause diseases like cancer. They are much more hesitant to extrapolate in the case of behavioral genes. Still, understanding the genetic basis of social behavior in animals is expected to cast some light on human behavior.

Last month researchers reported on the role of such genes in the sexual behavior of both voles and fruit flies. One gene was long known to promote faithful pair bonding and good parental behavior in the male prairie vole. Researchers discovered how the gene is naturally modulated in a population of voles so as to produce a spectrum of behaviors from monogamy to polygamy, each of which may be advantageous in different ecological circumstances.

The second gene, much studied by fruit fly biologists, is known to be involved in the male's elaborate suite of courtship behaviors. New research has established that a special feature of the gene, one that works differently in males and females, is all that is needed to induce the male's complex behavior.

Another Replication of Fine Particles and Mortality

Another replication of the association between particulate air pollution and mortality adds more weight to the evidence. This study comes from Johns Hopkins.The National Morbidity and Mortality Air Pollution Study includes data for 100 US cities, For the period 1987–2000, at the national level, a 10-µg/m3 increase in particulate matter less than 10 µm in aerodynamic diameter [PM10] at a 1-day lag was associated with 0.15%, 0.14%, 0.36%, and 0.14% increases in mortality for winter, spring, summer, and fall, respectively. An analysis by geographic region found a strong seasonal pattern in the Northeast (with a peak in summer) and little seasonal variation in the southern regions of the country. These results provide useful information for understanding particle toxicity and guiding future analyses of particle constituent data.

American Journal of Epidemiology 2005 161(6):585-594;

Seasonal Analyses of Air Pollution and Mortality in 100 US Cities

Roger D. Peng1, Francesca Dominici1, Roberto Pastor-Barriuso2, Scott L. Zeger1 and Jonathan M. Samet3

1 Department of Biostatistics, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD2 Epidemiology and Biostatistics Section, National Center for Epidemiology, Carlos III Institute of Health, Madrid, Spain3 Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD

High Rent Molecular Mechanisms Support Low Dose Chemical Carcinogenesis Risk

BrooklynDodger wades further into the uncharted swamp of fundamental mechanisms for carcinogenesis. All this stuff was invented after BrooklynDodger went to toxicology school; thus the Dodger warns this commentary to be metaphorical rather than grounded in deep knowledge of the field.

The Dodger reminds that importance of mechanism is whether a dose- [and implicitly exposure] response mechanism persists into the region where population effects can’t be directly observed. “Genotoxic” mechanisms are a type where a single deranged [initiated] cell progresses to a clone of malignant cells; thus, the relationship has no threshold [that is, no range where is the dose-response relationship is abolished.]

The Dodger previously blogged a Gaylor paper suggesting that carcinogens which enhance an underlying mechanism of carcinogenesis [this is a statistical paper, with none of this high rent molecular biology] will be linear to low doses.

BrooklynDodger further repeats that mutations – a putative mechanism of carcinogenesis – make for genes that don’t work [code for proteins that don’t work]. This frames mechanisms which turn off tumor prevention pathways.

p53 is a cell suicide [apoptotic] protein. BrooklynDodger will now have to learn what ATM, hTERT and TRF2h are.

BrooklynDodger notes that circulating lymphocytes are not the tumor. [Tumors sometimes have increased p53; the Dodger imagines this arises because the tumor cells are trying kill themselves and failing.] Biological plausibility for this observed association would be that whatever is reducing the protection in the lymphocytes also reduces the protection in the epithelial cells in the bladder.

As a token of common underlying mechanism, this paper supports low dose continuity of chemical carcinogenesis.

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Carcinogenesis 2005 26(10):1741-1747; doi:10.1093/carcin/bgi126


Roles of tumor suppressor and telomere maintenance genes in cancer and aging—an epidemiological study
Jian Gu, Margaret R. Spitz, Hua Zhao, Jie Lin, H.Barton Grossman 1, Colin P. Dinney 1 and Xifeng Wu *
Department of Epidemiology and 1 Department of Urology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX, USA
Advanced age is strikingly linked to increased incidence of cancer. … we used a case-control design and measured the mRNA expression levels of p53, ATM, hTERT and TRF2, the four major protectors of genomic integrity, in isolated peripheral blood lymphocytes from 202 confirmed bladder cancer (BC) patients and 199 healthy controls. … expressions of p53, ATM and TRF2 significantly decreased with advancing age in cases … In controls, however, p53 expression significantly increased with advancing age (P for trend = 0.05). Among subjects (image placeholder)65 years of age, the expressions of p53, ATM and TRF2 were significantly lower in cases than in controls … suggesting that attenuated genomic maintenance mechanisms lead to increased cancer risk in older individuals. …low p53 expression was associated with a significantly increased BC risk in older people … older subjects without detectable hTERT expression had a significantly reduced BC risk ... Our study provides the first epidemiologic evidence that the increased genomic instability resulting from the combination of telomere dysfunction, impaired ATM- and p53-mediated DNA damage, and/or telomere dysfunction response pathway contributes to increased cancer incidence in the elderly population.

Strike Reduces Pollution

BrooklynDodger blogs this abstract because it echoes the Pope study of air pollution in Utah: there the strike shut down a steel mill, here the strike shut down the busses. The investigators cite one study by Pope, but not the strike study.

BrooklynDodger personally has observed Sao Paulo busses, plumes of black smoke at street level are the rule, not the exception.

BrooklynDodger notes that busses are not the only source of pollution in SP. Also, the Dodger warns that mutagenicity of particles may not be the primary mechanism by which diesel particulate matter causes lung cancer.

Environmental Research 98 (2005) 1–7
Diesel emissions significantly influence composition and mutagenicity of ambient particles: a case study in Sao Paulo, Brazil
R. Carvalho-Oliveira,a R.M.K. Pozo,a D.J.A. Lobo,a A.J.F.C. Lichtenfels,a
H.A. Martins-Junior,b J.O.W.V. Bustilho,b M. Saiki,b I.M. Sato,b and P.H.N. Saldivaa,_
aLaboratory of Experimental Air Pollution, Department of Pathology, School of Medicine, Faculty of Medicine, University of Sa˜o Paulo,
Av. Dr. Arnaldo 455, CEP 01246-903 Sao Paulo, SP, Brazil
bInstitute of Energetic and Nuclear Research, University of Sa˜o Paulo, Av. Professor Lineu Prestes, 2242, CEP 05508-000 Sa˜o Paulo, SP, Brazil

In 2003, a bus strike paralyzed the fleet of buses in Sao Paulo, Brazil during 3 days, from 6 to 8 of April, the complete interruption of services being achieved on the 7th. We evaluated the effect of the absence of this source of pollution on the composition, mutagenicity, and toxicity of the fine particulate material collected during this period. Particles were sampled in glass fiber filters on days 7 and 15 of April of 2003 (strike and nonstrike days, respectively), using a high-volume sampler. Trace element determinations (As, Br, Co, Cl, Fe, La, Mn, Sb, Sc, and Th) of particulate material samples were carried out by neutron activation analysis. Sulfur determination was done by X-ray fluorescence analysis. The ratio between nonstrike/strike concentrations of hydrocarbons associated with automotive emissions (benzene, toluene, ethyl-benzene, and xylenes; BTEX) was determined by gas chromatography/mass spectrometry. Mutagenesis of testing solutions was determined by means of the Tradescantia micronucleus assay in early tetrads of Tradescantia pallida. The inhibition of mitosis of the cells of the primary meristema of the root tips of Allium cepa was used as an index of the toxicity. Fine particle trace element contents were lower during the strike. The concentrations of sulfur and BTEX were 50% and 39.3% lower, respectively, on the strike day. A significant (P < .038) reduction of micronuclei induced by fine particles sampled during the strike was observed. No effect of the strike on toxicity was detected. These results indicate that a program aiming to reduce emissions of the bus fleet in our town may impact positively the air quality by reducing the mutagenic potential of ambient particles.

Breast v. Bottle - Name Your Poison

BrooklynDodger previously blogged a paper showing that formula feeding was associated with greater BMI in later life compared to breast feeding. This paper, based on Spanish body burdens of organochlorines, shows that breast feeding is associated with higher body burdens of OC’s in early life, compared to formula feeding.

This is not exactly surprising.

Obviously, it needs to be considered whether these OC's are associated with any effect at these levels. The task of assessing effects in humans is complicated by the wide distribution of the exposures.

In some ways, concern for adverse effect of body burden of OC's or POP's is so '60s and Rachel Carson, while the new focus is fine, ultrafine or nanoparticles.

Maybe the OC’s are associated with the higher BMI’s in the other study?

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Environmental Research Volume 98, Issue 1 , May 2005, Pages 8-13

Breastfeeding and concentrations of HCB and p,p′-DDE at the age of 1 year
Núria Ribas-Fitóa, , , Joan O. Grimaltb, Esther Marcob, Maria Salaa, Carlos Mazónc and Jordi Sunyera aRespiratory and Environmental Health Research Unit, Institut Municipal d'Investigació Mèdica, C.Dr. Aiguader, 80, 08003 Barcelona, SpainbDepartment of Environmental Chemistry, CID-CSIC, Barcelona, SpaincPrimary Health Care Center of Flix, Tarragona, Spain Received 16 February 2004; revised 17 May 2004; accepted 27 May 2004. Available online 14 August 2004.
Abstract
Exposure to organochlorine compounds (OCs) occurs both in utero and through breastfeeding. Levels of hexachlorobenzene (HCB) in the cord serum of newborns from a population located in the vicinity of an electrochemical factory in Spain are among the highest ever reported. We aimed to assess the degree of breast milk contamination in this population and the subsequent exposure of children to these chemicals through breastfeeding. A birth cohort including 92 mother–infant pairs (84% of all births in the study area) was recruited between 1997 and 1999 in five neighboring villages. OCs were measured in cord serum, colostrum, breast milk, and children's serum at 13 months of age. Concentrations of OCs were detected and quantified in all colostrum and milk samples. The concentrations in mature milk were lower than those encountered in colostrum. At 13 months of age the highest concentration of OC was found for dichlorodiphenyl dichloroethane (p,p′-DDE), in contrast to what these children presented at birth, where HCB was the highest compound. Those infants who were breastfed had higher concentrations at the age of 1 than those who were formula fed (2.13 ng/mL of HCB among formula feeders vs 4.26 among breast feeders, and 1.95 of p,p′-DDE vs 6.00 (P<0.05)). Long-term breastfeeding leads to a dose–response increase of the concentrations in children's serum during the first year of life.

Back to Woodstock - Flawed Census Tract Epi and Asbestos in Water

Another exercise in census tract epidemiology, which could have been reviewed and edited better, concerns water contamination with asbestos fibers. The “feel good” “don’t worry, be happy” abstract is common for technical reports by public health authorities, but might have been better stated for a scientific publication.

GI exposure to asbestos is a meaningful issue. Rats don’t get GI tumors from eating quite a lot of asbestos, but you need to gas rats with a thousand fibers/cc to get meaningful lung tumor yield. The rat’s a lousy model for colorectal tumors, also.

Backstory: Water service goes down. “Following flushing of the water mains ,five water samples were collected from different locations in the Woodstock water supply. Four of the samples had asbestos levels greater than 10 million fibers per liter (MFL), with the maximum equaling 304.5 MFL. Over 90% of the asbestos was chrysotile; the remainder was crocidolite (Webber and Covey,1991 ).”

It would have been nice had the NYS Public Health Department provided some asbestos in water data for other than this special circumstance. Most likely there’s none because of “don’t ask, don’t tell, don’t pursue.”

Literature review: “Cancer incidence or mortality has been examined in eight populations exposed to asbestos in drinking water in the United States,Canada , and Norway …An excess of stomach cancer, primarily among males, was observed in five study populations …,and pancreatic cancer was associated with exposure among males in one population and among females in another. A positive association was not reported for more than one study population for any other cancer site.”

BrooklynDodger previously blogged, more than once, that census tract epidemiology aimed at a specific source or agent is a lose-lose scientific proposition. Absence of association is expected because these studies are likely powerless, and associations found are unlikely due to the target exposure, for the same reason.

Here, results are standardized incidence rates, adding shakiness. This blocks comparing overall mortality, to see if there is a “healthy community effect” similar to the healthy worker effect, an artifact of the method. All cancer incidence was 0.91 for the men, 0.96 for the women. Were this a big enough study to find anything, proportional cancer incidence ratios might be a more reliable indicator of excess.

Total GI cancers had Upper Confidence Intervals of 1.26 for the women and 1.63 for the men. Nevertheless, the investigators stumbled on a 3-fold significant excess of pancreatic cancer among men, with a whopping UCI. They Houdini this finding with a totally powerless residence duration response analysis for total GI [not in excess anyway] and total respiratory cancer.

No mesotheliomas were observed. The investigators might have given BrooklynDodger an expected or a confidence interval to see what level of risk had been ruled out.

What frosts the Dodger is that the editors let this line in the abstract: “This association may be related to factors other than asbestos exposure such as occupation and lifestyle or to chance.” Talk about conveying negative information [i.e., stuff that makes you know less after you have read it.]

Bottom line, this study was inadequate to assess the association between drinking water and cancer in Woodstock, or asbestos in drinking water. Nevertheless, there is equivocal evidence for an association of being in this cohort and increased risk of pancreatic cancer.


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Environmental Research 98 (2005) 224–232
Cancer incidence and asbestos in drinking water,Town of Woodstock,New York,1980–1998

Marilyn L. Brownea,_,Deepa Varadarajulub,Elizabeth L. Lewis-Michla, Edward F. Fitzgeralda a

New York State Department of Health, Bureau of Environmental and Occupational Epidemiology, 547 River St. Rm. 200, Troy, NY 12180, USA bNew York State Department of Health, Bureau of Chronic Disease Epidemiology and Surveillance, Albany, NY 12237,
USA

Abstract Late in 1985,asbestos contamination was discovered in the public water supply of the Town of Woodstock, Ulster County ,New York. Contamination resulted from asbestos–cement pipes installed in the town water system in the mid to late 1950s and the corrosiveness of the local water. The New York State (NYS) Department of Health established the Woodstock Asbestos Exposure Registry (WAER) in 1986 to monitor rates of cancer among individuals who lived on the water supply between 1960 and 1985. Demographic ,health, and residential information were collected on 2936 registrants. The follow-up period for observation of cancer was 1980–1998, consistent with the expected lag of 20–30+ years for development of asbestos-related cancers. The NYS Cancer Registry was used to ascertain cancer diagnoses. Standardized incidence ratios (SIRs) for gastrointestinal, respiratory,and total cancers were all approximately 1.00 or less and all 95% confidence intervals (CIs) included 1.00. For individual types of the gastrointestinal cancers ,only the SIR for pancreatic cancer was marginally statistically significant at 2.19 (95% CI=1.00–4.16), based on a total of nine observed cases. The excess in pancreatic cancer occurred primarily among men (SIR=3.08; 95% CI=1.13–6.70) and was only slightly elevated among women (SIR=1.39; 95% CI=0.29–4.06). This association may be related to factors other than asbestos exposure such as occupation and lifestyle or to chance. No cases of mesothelioma were observed among WAER participants. There was no increase in incidence by latency or duration of residence on the water supply, but the ability to detect these trends is limited by small numbers and unknown dates of initial exposure. The general pattern of results did not demonstrate a likely link between exposure to asbestos in drinking water and cancer occurrence among participants in the WAER.

Inner City Indoor Air

BrooklynDodger posts this abstract as a not quite random sample of indoor air exposures in inner city dwellings, almost all row houses. This informs population studies of health effects of outdoor air pollution.

The houses were recruited because there was a kid with asthma living there, but there were no control kids or houses. BrooklynDodger could imagine the asthma houses were worse, but it’s safer to think these are random.

There’s a table about house observations: most kitchens had dishes in the sink [as in BrooklynDodger’s domicile]; there was lot of water intrusion; 20% dogs, 26% cats…Mice droppings were found in 38% of kitchens. [Occasionally in BD’s domicile, but not every day.]

About 75% of the PM mass is PM 2.5 [BrooklynDodger expects most of this is really PM 1.0]. The 25th percentile PM 2.5 exceeded the EPA 24-hour average limit of15 ug/M3. BrooklynDodger expects that a lot of the excess over outdoor measured PM is indoor smoking, although rooftop vs. street level may also contribute. The investigators noted that PM levels were higher in the evening.

Regarding allergens:

“The most commonly detected allergen was mouse, found in all the bedroom samples and in 99% of kitchen samples. Cockroach, dog, and cat allergens were also common, while house dust mite was less common. The predominant house dust mite allergen, Der f 1, was detected in 59% of bedroom samples, but the median concentration was only 66 ng/g. Mouse allergen was also found in large quantities, with a median concentration in bedroom dust (3659 ng/g) that was an order of magnitude higher than cat or dog allergen. Median concentrations of cockroach allergen were highest in the kitchen (22 U/g), followed by the living room (median 5.2 U/g) and bedroom (4.5 U/g).”


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Environmental Research 98 (2005) 167–176
Indoor exposures to air pollutants and allergens in the homes of asthmatic children in inner-city Baltimore
Patrick N. Breyssea,_, Timothy J. Buckleya, D’Ann Williamsa, Christopher M. Becka,
Seong-Joon Joa, Barry Merrimanb, Sukon Kanchanaraksac, Lee J. Swartzd, Karen
A. Callahand, Arlene M. Butzd, Cynthia S. Randb, Gregory B. Dietteb, Jerry A. Krishnanb,
Adrian M. Moseleye, Jean Curtin-Brosnand, Nowella B. Durkind, Peyton A. Egglestond
aDepartment of Environmental Health Sciences, Johns Hopkins Bloomberg School of Public Health, 615 North Wolfe Street Room W6010A, Baltimore,
MD 21205, USA
bDepartment of Pulmonary Medicine, School of Medicine, Johns Hopkins University, Baltimore, MD 21205, USA
cDepartment of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 21205, USA
dDepartment of Pediatrics, School of Medicine, Johns Hopkins University, Baltimore, MD 21205, USA
eThe Johns Hopkins Health System, Baltimore, MD 21205, USA
…
This paper presents indoor air pollutant concentrations and allergen levels collected from the homes of 100 Baltimore city asthmatic children participating in an asthma intervention trial... Dust allergen samples were collected from the child’s bedroom, the family room, and the kitchen. The mean PM10 concentration, 56.5 ug/m3… the PM2.5 concentration … 45.1ug/m3. … Smoking households’ average PM2.5 and PM10 concentrations are 33–54 mg/m3 greater than those of nonsmoking houses, with each cigarette smoked adding 1.0 mm/m3 to indoor PM2.5 and PM10 concentrations. Large percentages of NO2 and O3 samples, 25% and 75%, respectively, were below the limit of detection. The mean NO2 indoor concentration is 31 ppb, while the mean indoor O3 concentration in the ozone season was 3.3… ppb. …

Broken Down by Age

Epidemiologists are defined as health scientists broken down by age and sex.

As BrooklynDodger gets on in years, the Dodger starts to look at health effects in the elderly, beyond those of alcohol. This paper frustrated the Dodger, since it never gave the base rate of depression, on a bunch of coefficients. Living in a poor neighborhood increased the risk of depressive symptoms, more elderly people in the neighborhood reduced the risk. Amenities had no effect.

The paper quoted a range of 10 to 27% of free living elderly with depressive symptoms.

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American Journal of Epidemiology 2005 162(3):253-260;

Neighborhood Contextual Influences on Depressive Symptoms in the Elderly
Laura D. Kubzansky, S. V. Subramanian, Ichiro Kawachi, Martha E. Fay, Mah-J. Soobader and Lisa F. Berkman
From the Department of Society, Human Development, and Health, Harvard School of Public Health, Boston, MA
Reprint requests to Dr. L. Kubzansky, Department of Society, Human Development, and Health, Harvard School of Public Health, 677 Huntington Avenue, Boston, MA 02115-6096 (e-mail: lkubzans@hsph.harvard.edu (image placeholder)).

… This study used … data from the New Haven component of the Established Populations for Epidemiologic Studies of the Elderly, a community-based sample of noninstitutionalized men and women aged 65 years or older and living in the city of New Haven, Connecticut, in 1982. Neighborhoods were characterized by census-based characteristics and also by measures of the neighborhood service environment using data abstracted from the New Haven telephone book Yellow Pages. Living in a poor neighborhood was associated with higher levels of depressive symptoms in older adults, above and beyond individual vulnerabilities. In addition, the presence of more elderly people in the neighborhood was associated with better mental health among older adults. The authors found no evidence that access to services hypothesized to promote social engagement, to provide health services, or to affect the reputation of a neighborhood explained (i.e., mediated) neighborhood variations in depressive symptoms

Fire last time

Now that we know that WTC workers and community residents were sickened by their exposures, it’s worth looking back at what those exposures were. This NIOSH paper recounting 1200 bulk and air samples, confirms again that exposures were less than [actually much less than] OSHA limits.

BrooklynDodger is willing to be convinced that the combination of exposures – smoke and dust together – is more toxic than either alone, or that some not usually measured contaminant – particles larger than PM 10 – caused the observed effects. It’s more radical to say that the PM 2.5 [or respirable fraction] PEL should be lowered to less than 100 micrograms/M3

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Toxicol Ind Health. 2001 Jun;17(5-10):247-53.
Occupational exposures during the World Trade Center disaster response.Wallingford KM, Snyder EM.National Institute for Occupational Safety and Health 4676 Columbia Parkway (R-11), Cincinnati, Ohio 45226, USA. kwallingford@cdc.govUpon the request of the New York City Department of Health, the Centers for Disease Control and Prevention's National Institute for Occupational Safety and Health (NIOSH) monitored occupational exposures among emergency response workers during the rescue and recovery activities at the World Trade Center disaster site from September 18 through 4 October 2001. During this period, over 1,200 bulk and air samples were collected to estimate or characterize workers' occupational exposures. Samples were collected and analyzed for asbestos, carbon monoxide (CO), chlorodifluoromethane (Freon 22), diesel exhaust, hydrogen sulfide, inorganic acids, mercury and other metals, polynuclear aromatic hydrocarbons, respirable particulate not otherwise regulated (PNOR), respirable crystalline silica, total PNOR, and volatile organic compounds. Exposures to most of these potential hazards did not exceed NIOSH Recommended Exposure Limits or Occupational Safety and Health Administration Permissible Exposure Limits. However, one torch cutter was overexposed to cadmium and another worker (and possibly three others) was overexposed to CO. The elevated cadmium and CO levels were the result of workers using oxy-acetylene cutting torches and gasoline-powered cutting saws. Recommendations were made to ensure adequate ventilation and worker understanding when using these tools and, where possible, to substitute rechargeable, battery-powered cutting saws for gasoline-powered ones.

Health Effects Among WTC Recovery Site Workers

BrooklynDodger returns to 9/11 and the World Trade Center site.

This paper comes from Johns Hopkins, adding yet another team of investigators.

Repeating previous posts, exposures were well below OSHA limits for everything, except for welders who were almost all in compliance but had scattered exposures at or near the OSHA limit.

Employees were truck drivers, laborers, carpenters, and heavy equipment operators. No welders [ironworkers] or firefighters. The text is unclear on the subjects arrival date at the site. Tests were conducted 3 months into the event, some employees appeared to have been there from the early days, but clearly after the initial collapse and cloud of large particle dust.

“Among the 183 workers who Participated in this study, 52% reported nasal congestion, 43% reported sore throat, and 44% reported experiencing a hoarse throat while working at the site. Of the 119 workers who began working at the site with no previous history of lower respiratory symptoms, 34% developed a new cough, 24% reported new phlegm production, and 19% reported new wheeze.”

The investigators had no data on pre- and post- PFT’s. Those with symptoms had lower PFT’s than those without.

Another independent data point showing effects well below the OSHA PEL’s.

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Respiratory effects of inhalation exposure among workers during the clean-up effort at the World Trade Center disaster site.

Herbstman JB, Frank R, Schwab M, Williams DL, Samet JM, Breysse PN, Geyh AS.

Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 21205, USA.

During December 2001 we conducted a field study of 183 clean-up and recovery workers at the World Trade Center (WTC) disaster site to assess respiratory health effects potentially resulting from their work at the site. On site, we administered a respiratory health questionnaire designed to assess upper respiratory symptoms and lower respiratory symptoms, including cough, phlegm, and wheeze, as well as indices of exposure, including number of days worked at the site and job category. Spirometry was conducted for 175 workers. Sixty-five percent of the workers surveyed arrived at the site without lower respiratory symptoms. Of this group, 34% developed cough, 24% developed phlegm, and 19% developed wheeze. Prevalence rates of these symptoms were related to the number of days spent working at the WTC, but not job category. The mean percentage predicted FEV(1) and FVC were 6% and 5% lower, respectively, for workers who developed new lower respiratory symptoms compared to those who remained symptom free. While the development of new wheeze suggested the presence of airway obstruction, the near-normal distribution of age-adjusted FEV(1)/FVC ratios suggested that the degree of obstruction was mild. The prevalence rates of upper airway symptoms (nasal congestion, sore throat, hoarse throat) exceeded those of lower respiratory symptoms, however, it was not determined whether symptoms pre-dated arrival at the WTC site.

Breast Feeding Prevents Overweight?

The Leche league validated. Or, maybe McDonalds can breath easier. Seventeen studies were found meeting inclusion criteria. Statistical significant reduction in risk of overweight was found for any breast feeding. The risk of overweight declined to 0.68 for greater than 9 months. Maybe the endemic of overweight decried by CDC is really due to decline in breast feeding.

BrooklynDodger was not interested enough to get the full text to see the discussion of confounding, which is the first concern with any data of this kind. Weight at exit from breast feeding compared to formula babies would be nice to know. The Dodger is hard pressed to figure biological plausibility.

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American Journal of Epidemiology 2005 162(5):397-403; doi:10.1093/aje/kwi222


American Journal of Epidemiology Copyright © 2005 by the Johns Hopkins Bloomberg School of Public Health All rights reserved
(image placeholder)


Duration of Breastfeeding and Risk of Overweight: A Meta-Analysis
Thomas Harder1, Renate Bergmann1, Gerd Kallischnigg2 and Andreas Plagemann1
1 Clinic of Obstetrics, Division of Experimental Obstetrics, Charité—University Medicine, Berlin, Germany2 Epidemiology Research Group, Institute of Public Health, Technical University, Berlin, Germany
Reprint requests to Dr. Thomas Harder, Clinic of Obstetrics, Division of Experimental Obstetrics, Campus Virchow-Klinikum, Charité—University Medicine Berlin, Augustenburger Platz 1, 13353 Berlin, Germany (e-mail: thomas.harder@charite.de (image placeholder)).
Observational studies suggest a longer duration of breastfeeding to be associated dose dependently with a decrease in risk of overweight in later life. The authors performed a comprehensive meta-analysis of the existing studies on duration of breastfeeding and risk of overweight. Studies were included that reported the odds ratio and 95% confidence interval (or the data to calculate them) of overweight associated with breastfeeding and that reported the duration of breastfeeding and used exclusively formula-fed subjects as the referent. Seventeen studies met the inclusion criteria. By meta-regression, the duration of breastfeeding was inversely associated with the risk of overweight (regression coefficient = 0.94, 95% confidence interval (CI): 0.89, 0.98). Categorical analysis confirmed this dose-response association (<1 month of breastfeeding: odds ratio (OR) = 1.0, 95% CI: 0.65, 1.55; 1–3 months: OR = 0.81, 95% CI: 0.74, 0.88; 4–6 months: OR = 0.76, 95% CI: 0.67, 0.86; 7–9 months: OR = 0.67, 95% CI: 0.55, 0.82; >9 months: OR = 0.68, 95% CI: 0.50, 0.91). One month of breastfeeding was associated with a 4% decrease in risk (OR = 0.96/month of breastfeeding, 95% CI: 0.94, 0.98). The definitions of overweight and age had no influence. These findings strongly support a dose-dependent association between longer duration of breastfeeding and decrease in risk of overweight.

9/11 was fire and dust - community effects

9/11 was fire, and dust.  Katrina is water and sludge.  For the population and recovery workers, the problem is describing the exposure and the potential health effects of exposure.  It’s time to look back on 9/11 as data finally is reaching the literature.
This study combines forces of the NY State Department of Health, NYU and SUNY Albany.
Compared to upper NYC residents, the WTC area residents suffered about twice [or more than twice] the adverse outcomes, based on questionnaires.  Response rates in both areas to mailed questionnaires was about 23%.    
Whatever persons were exposed to, it’s clearly an effect level.  But what was the exposure?
Unfortunately, this paper did not seek exposure data.  EPA PM 10 and PM 2.5 exposure data, largely collected at rooftop levels, would have been available on an hourly basis from multiple sites in each locality.  Both sampling methods exclude large particles, which may be the cause of continuing rhinitis among workers.  Rooftop locations may exclude the large particles as well.
The same issue of AJE includes a critique and response, largely over the issue of response bias.  BrooklynDodger believes the authors win the argument on the results not being the result of such bias.
Now that the effect is known, it would be of value for someone to collect as much ground level and indoor sampling data as can be found, and reconstruct the exposures.
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American Journal of Epidemiology 2005 162(6):499-507; doi:10.1093/aje/kwi233
Upper Respiratory Symptoms and Other Health Effects among Residents Living Near the World Trade Center Site after September 11, 2001
Shao Lin1, Joan Reibman2, James A. Bowers1, Syni-An Hwang1, Anne Hoerning2, Marta I. Gomez1 and Edward F. Fitzgerald3
1 Center for Environmental Health, New York State Department of Health, Troy, NY2 Department of Medicine, Division of Pulmonary and Critical Care Medicine, New York University School of Medicine, New York, NY3 Department of Epidemiology and Biostatistics, School of Public Health, University at Albany, State University of New York, Renssalaer, NY
Correspondence to Dr. Shao Lin, Bureau of Environmental and Occupational Epidemiology, New York State Department of Health, 547 River Street, Room 200, Troy, NY 12180 (e-mail: sxl05@health.state.ny.us (image placeholder)).
The authors investigated changes in respiratory health after September 11, 2001 ("9/11") among residents of the area near the World Trade Center (WTC) site in New York City as compared with residents of a control area. In 2002, self-administered questionnaires requesting information on the presence and persistence of respiratory symptoms, unplanned medical visits, and medication use were sent to 9,200 households (22.3% responded) within 1.5 km of the WTC site (affected area) and approximately 1,000 residences (23.3% responded) in Upper Manhattan, more than 9 km from the site (control area). Residents of the affected area reported higher rates of new-onset upper respiratory symptoms after 9/11 (cumulative incidence ratio = 2.22, 95% confidence interval (CI): 1.88, 2.63). Most of these symptoms persisted 1 year after 9/11 in the affected area. Previously healthy residents of the affected area had more respiratory-related unplanned medical visits (prevalence ratio = 1.73, 95% CI: 1.13, 2.64) and more new medication use (prevalence ratio = 2.89, 95% CI: 1.75, 4.76) after 9/11. Greater impacts on respiratory functional limitations were also found in the affected area. Although bias may have contributed to these increases, other analyses of WTC-related pollutants support their biologic plausibility. Further analyses are needed to examine whether these increases were related to environmental exposures and to monitor long-term health effects.

Apologies for Hiatus

Out of town over the holiday

Short Thin Asbestos Fibers and Mesothelioma

BrooklynDodger was raised in the era when students were taught to wonder why asbestos caused fibrosis and lung cancer, while silica only fibrosis. Now, silica is also known to be carcinogenic to humans. Within asbestos risk assessment, long fibers were thought to be the hazard, with short fibers to be ignored. That’s the “Stanton” hypothesis. There’s also the claim that chrysotile asbestos [white asbestos from the great white north] while the nasty amphiboles that no one uses anymore were the hazard.

You would think by now that everything was known about asbestos, and especially everything about asbestos and mesothelioma. Not so, important new data are being published even now.

These investigators got tissue from 168 mesothelioma victims. The investigators found “(1) long, thin asbestos fibers consistent with the Stanton hypothesis comprised only 2.3% of total fibers (247 / 10,575) in these tissues; (2) the majority (89.4%) of the fibers in the tissues examined were shorter than or equal to 5 microm in length (9454 of 10,575), and generally (92.7%) smaller than or equal to 0.25 microm in width (9808 of 10,575). (3) Among asbestos types detected in the lung and mesothelial tissues, chrysotile was the most common asbestos type to be categorized as short, thin asbestos fibers...”

The full text wouldn’t download to see if there were cases with no crocidolite or amosite fibers. And whether any of the mesothelioma victims had no asbestos in tissue.

The occupational health issue revolves around correlation of the long fibers seen on phase contrast microscopy and the short thin fibers which are invisible in environmental sampling. Figuring out the small fiber exposure where PCM gives non detectable results is still an issue.


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Int J Hyg Environ Health. 2005;208(3):201-10.

Short, thin asbestos fibers contribute to the development of human malignant mesothelioma: pathological evidence.

Suzuki Y, Yuen SR, Ashley R.

Department of Community and Preventive Medicine, Mount Sinai School of Medicine, 1 Gustave L. Levy Place, Box 1057, New York, NY 10029, USA. yasunosuke.suzuki@mssm.edu

Based on animal studies, long and thin asbestos fibers (> or =8 microm in length and < or = 0.25 microm in width) have been postulated to be strongly carcinogenic inducing pleural malignant mesothelioma, while shorter, thicker fibers have been postulated to pose a lesser risk (Stanton hypothesis). The objective of this study is to test the validity of the Stanton hypothesis through direct pathologic analysis of human mesothelioma tissue. Digested bulk tissue samples, or ashed 25 microm thick sections, or both, were prepared from lung and mesothelial tissues taken from 168 cases of human malignant mesothelioma. In these tissues, 10,575 asbestos fibers (4820 in the lung and 5755 in mesothelial tissues (1259 in fibrotic serosa and 4496 in mesotheliomatous tissue)) were identified by high-resolution analytical electron microscopy. Dimensions of these asbestos fibers were measured in printed electron micrographs. Results were as follows: (1) long, thin asbestos fibers consistent with the Stanton hypothesis comprised only 2.3% of total fibers (247 / 10,575) in these tissues; (2) the majority (89.4%) of the fibers in the tissues examined were shorter than or equal to 5 microm in length (9454 of 10,575), and generally (92.7%) smaller than or equal to 0.25 microm in width (9808 of 10,575). (3) Among asbestos types detected in the lung and mesothelial tissues, chrysotile was the most common asbestos type to be categorized as short, thin asbestos fibers. (4) Compared with digestion technique of the bulk tissue, ashing technique of the tissue section was more effective to detect short, thin fibers. We conclude that contrary to the Stanton hypothesis, short, thin, asbestos fibers appear to contribute to the causation of human malignant mesothelioma. Such fibers were the predominant fiber type detected in lung and mesothelial tissues from human mesothelioma patients. These findings suggest that it is not prudent to take the position that short asbestos fibers convey little risk of disease.