Wednesday, December 31, 2008

Ash Hills and Arsenic
High Arsenic Levels Found in Water Near Tenn. Ash Spill

By Kristin M. Hall Associated Press Tuesday, December 30, 2008; Page A03

KINGSTON, Tenn., Dec. 29 -- Some water samples near a massive spill of coal ash in eastern Tennessee are showing high levels of arsenic, and state and federal officials Monday cautioned residents who use private wells or springs to stop drinking the water...


BrooklynDodger(s) comment: Maybe you don't think about coal ash much, the Dodger(s) certainly didn't. What is "clean coal" anyway? The starting point of musing was that whatever stuff is in the coal that doesn't form gaseous combustion products is left behind as ash. And the coal contains whatever was in the trilobites and trees of way back when. Since living creatures contain metals, burned creatures leave behind metal oxides, which yield a high pH. Remember saponification of fats to soaps by soda ash?

But a longer-than-intended wander through google yielded some background information. The Dodger(s) invite corrections and additions to this information.

Most of us know that arsenic is known to be a human carcinogen by inhalation and by ingestion in drinking water. IARC opines "There is sufficient evidence in humans that arsenic in drinking-water causes cancers of the urinary bladder, lung and skin." The full text of this monograph can be found at In press accounts, this classification is characterized as "has been linked to cancer" which reads much weaker than an alternative which might be "arsenic in actual drinking water people drink has caused bladder, lung and skin cancer."

The EPA MCL limit for arsenic in drinking water is 10 ppb (10 ug/L) with a goal of zero. There appear to be no EPA limits for arsenic in soil; cleanup levels are triggered by site specific considerations. Most coal ash is fly ash, there is considerable effort to finding what to do with it, although it is not deemed hazardous waste. There's even a "flyashinfo" web site. Which contains some technical papers.

According to the site, most fly ash is <>

Tuesday, December 30, 2008

Formaldehyde - You Get What You Model For

Sensitivity Analysis of Biologically Motivated Model for Formaldehyde-Induced Respiratory Cancer in Humans

Annals of Occupational Hygiene 2008 52(6):481-495; doi:10.1093/annhyg/men038

Kenny S. Crump1,3,*, Chao Chen2, John F. Fox2, Cynthia Van Landingham1 and Ravi Subramaniam2
1 ENVIRON International Corporation, 1900 North, 18th Street, Suite 804, Monroe, LA 71201, USA2 National Center for Environmental Assessment, Office of Research and Development, US Environmental Protection Agency, Mail Code 8623D, 1200 Pennsylvania Avenue, NW, Washington, DC 20460, USA

"Conolly et al. (2003, 2004) developed biologically motivated models of formaldehyde carcinogenicity in F344 rats and humans based on a two-stage clonal expansion model of cancer. Based on the human model, Conolly et al. (2004) claimed that cancer risks associated with inhaled formaldehyde are deminimis at relevant human exposure levels. However, they did not conduct a sensitivity analysis to evaluate the robustness of this conclusion. Here, we present a limited sensitivity analysis of the formaldehyde human model. We show that when the control animals from the National Toxicology Program (NTP) studies are replaced with control animals only from NTP inhalation studies, estimates of human risk are increased by 50-fold. When only concurrent control rats are used, the model does not provide any upper bound (UB) to human risk. No data went into 20 the model on the effect of formaldehyde on the division rates and death rates of initiated cells. We show that slight numerical perturbations to the Conolly et al. assumptions regarding these rates can be made that are equally consistent with the underlying data used to construct the model, but produce estimates of human risk ranging anywhere from negative up to 10 000 times higher than those deemed by Conolly et al. to be ‘conservative’. Thus, we conclude that estimates of human risk by Conolly et al. (2004) are extremely sensitive to modeling assumptions. This calls into question the basis for the Conolly et al. claim of de minimis human risk and suggests caution in using the model to derive human exposure standards for formaldehyde"

BrooklynDodger(s) comment: There's something up with formaldehyde at EPA. The Dodger(s) believe this activity responds to a TSCA Section 21 Petition by NRDC asking for a rule; EPA denied the petition but announced an assessment. Previously the Dodger(s) have noted the drastic contrasts between inhalation exposure limits by OSHA, NIOSH, ACGIH, and ATSDR, in the context of Katrina trailers and other domicilary exposures. EPA has not set a reference concentration for formaldehyde, having last published an assessment of formaldehyde in IRIS in 1991 which contains a drinking water limit and a cancer unit risk value.

The EPA 1991 (before IARC reclassified formaldehyde as "KNOWN" to be carcinogenic to humans) assessment was:

B1 (Probable human carcinogen - based on limited evidence of carcinogenicity in humans)

Weight-of-Evidence Narrative: Based on limited evidence in humans, and sufficient evidence in animals. Human data include nine studies that show statistically significant associations between site-specific respiratory neoplasms and exposure to formaldehyde or formaldehyde-containing products. An increased incidence of nasal squamous cell carcinomas was observed in long-term inhalation studies in rats and in mice. The classification is supported by in vitro genotoxicity data and formaldehyde's structural relationships to other carcinogenic aldehydes such as acetaldehyde. This may be a synopsis of the full weight-of-evidence narrative. See IRIS Summary.

Quantitative Estimate of Carcinogenic Risk from Oral Exposure Not Assessed under the IRIS Program.

Quantitative Estimate of Carcinogenic Risk from Inhalation Exposure Inhalation Unit Risk(s) Extrapolation Method 1.3 x10-5 per ug/m3 Linearized multistage procedure, additional risk

The Dodger(s) will discuss this at a later time. You haven't heard the last from the Dodger(s) on formaldehyde (or anything else.) Staff from the Chemical Industry Institute of Toxicology (CIIT), now rebranded as the "Hamner Institute for Life Sciences," had published a risk assessment to compete with the EPA quantitative exposure response relationship. The publication above appears to represented an EPA alternative to the CIIT alternative to the EPA calculations. The key finding was that plausible alternative parameters to the CIIT parameters generated unit risks ranging from less than the CIIT estimate to 10,000 higher.

Monday, December 29, 2008

The Organization formerly Known as CIIT Gets Grant from EPA to Study Asbetos Toxicity

BrooklynDodger(s) comment: Vermiculate in Libby, Montana is a major concern for EPA, especially figuring out remediation in a town likely heavily contaminated. The Libby asbestos is amphibole, like crocidolite and amosite. Most asbestos to which people are and were exposed is a serpentine mineral, crysotile. Increased potency estimates for amphiboles relative to crysotile would much reduce the legacy risks and costs of asbestos. But also trigger greater cleanup efforts in Libby. In addition, estimates increasing the potency of long fibers and suggesting short fibers to be relatively impotent would reduce the legacy risks and costs of brake shoes.

Recently, EPA floated an "approach" to risk assessment that would greatly increase the relative potency of amphiboles and long fibers. The approach was rejected by the EPA Science Advisory Committee, for the second time.

The Dodger(s) will comment on the limited public health value of more mechanistic research on asbestos fiber types in future posts. For now, the Dodger(s) suggest that the more approapriate agency to receive this contract was the National Toxicology Program.$2%201%20Million%20EPA%20Grant%20to%20Study%20Asbestos%20121908.pdf

The Hamner Institutes for Health Sciences Receives
$2.1 Million Asbestos Research Grant
Environmental Protection Agency Awards Organization Funding To Study Inhaled Vermiculite Fiber

The three-year study will include assembling an inhalation exposure system for the exposure of fibers to laboratory animals, conducting range-finding and definitive toxicity studies in rats, and analyzing fiber content of rat tissues following exposure. The study will be led by four key personnel at The Hamner: Darol E. Dodd, Ph.D., DABT; Owen R. Moss, Ph.D; Ed Bermudez, M.S., DABT; and Brian A. Wong, Ph.D."

Sunday, December 28, 2008

Exposure to POP's Via Breast Milk

Lifestyle and polybrominated diphenyl ethers in human milk in the United States: A pilot study
Authors: Judy S. LaKind ab; Cheston M. Berlin Jr bc; Jennifer L. Stokes b; Daniel Q. Naiman d; Ian M. Paul b; Donald G. Patterson Jr e; Richard S. Jones e; Sarah Niehser e; Richard Y. Wang e; Larry L. Needham e; Matthew N. Lorber f; Andreas Sjdin e
Toxicological & Environmental Chemistry, Volume 90, Issue 6 November 2008 , pages 1047 - 1054

"Polybrominated diphenyl ethers (PBDE) are a class of brominated flame retardants with some congeners having the ability to accumulate in body lipids. The incorporation of PBDE in consumer products found primarily in the indoor environment suggests that routes of exposure include inhalation of indoor air and contact with indoor dust. The purpose of this study was to test the hypothesis that lifestyle factors, and in particular the proximity and use of products likely to contain PBDE in the indoor environment, are primarily responsible for levels of PBDE found in human milk. Human milk samples were taken from two populations of lactating women in the same geographic region of the United States: one “typical” of US suburban lifestyle, and the other practicing a traditional Amish lifestyle, which excludes many modern amenities containing PBDE, such as computers and televisions. For a subset of the cohort, persistent organic pesticides and polychlorinated biphenyls (PCB) were also measured in human milk samples. Despite the small number of participants, there is evidence suggestive of Amish women having lower PBDE concentrations in their milk. In addition, the nonsignificant differences in levels of PCBs and pesticides between the two groups of women as compared to the significant differences in levels of PBDE suggest an important route of exposure for PBDE other than diet. Information prepared for study participants is provided to initiate a dialogue on how to best communicate biomonitoring findings to study participants and to the public in general.
BrooklynDodger(s) comment: The object of this study was to detect exposure to brominated flame retardents. Humans are at the top of the food chain, so bioconcentration would be expected. Mobilization of POP's from lipid stores through the blood to human breast milk is also expected. Obviously the target population of infants is expected the most vulnerable. The paper suggests a human milk monitoring program may be helpful in tracking human exposure to POP's. Another finding less emphasized is that Amish lifestyle conferred no protection against PCB's and pesticides. >>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>

Saturday, December 27, 2008

Physical Activity and Breast Cancer - What About Work?

BrooklynDodger(s) comment: Very few chemicals have been associated with increased breast cancer. This is because most non-drug, non-hormonal agents have been found associated with cancer among workers with substantially higher exposure than the general population. However, there are relatively few women in such cohorts, and so little has come from these studies. Another reason may be inferred from this study. The study found that increased physical activity was associated with decreased breast cancer - a frequently observed effect which translates to a blame the victim tone in the standard cancer control literature ("You got cancer because you were lazy.")

Note that modest amounts of physical activity which conferred protection, "The most physically active group (who walked for 1 hour per day and exercised for 1 hour per week)" Compare that with standing and walking 10 hours a day, pounding steel on the assembly line. So women in industrial and construction occupations would be expected to present with a much reduced risk of breast cancer compared to the general population. Studies of industrial cohorts which might observe breast cancer rates close to expected should be considered studies finding an association between the exposure and breast cancer.


Effect of Physical Activity on Breast Cancer Risk: Findings of the Japan Collaborative Cohort Study

Sadao Suzuki1, Masayo Kojima1, Shinkan Tokudome1, Mitsuru Mori5, Fumio Sakauchi5, Yoshihisa Fujino6, Kenji Wakai2, Yingsong Lin7, Shogo Kikuchi7, Koji Tamakoshi3, Hiroshi Yatsuya4, Akiko Tamakoshi7 for the Japan Collaborative Cohort Study Group
"Purpose: This study aimed to examine prospectively the association between physical activity and breast cancer risk in a non-Western population.
Methods: We analyzed data from the Japan Collaborative Cohort Study, which included 30,157 women, ages 40 to 69 years at baseline (1988-1990), who reported no previous history of breast cancer, and provided information on their walking and exercise habits. The subjects were followed prospectively from enrollment until 2001 (median follow-up period, 12.4 years). Breast cancer incidence during this period was confirmed using records held at population-based cancer registries. The Cox proportional hazards model was used to estimate the hazard ratio (HR) for the association of breast cancer incidence with physical activity.
Results: During the 340,055 person-years of follow-up, we identified 207 incident cases of breast cancer. The most physically active group (who walked for 1 hour per day and exercised for 1 hour per week) had a lower risk of breast cancer (HR, 0.45; 95% confidence interval, 0.25-0.78) compared with the least active group after adjusting for potential confounding factors. The inverse association of exercise on breast cancer was stronger among those who walked for 1 hour per day than those who walked for <1 p =" 0.042).">
Conclusions: Our analysis provided evidence that physical activity decreased the risk of breast cancer. Walking for 1 hour per day and undertaking additional weekly exercise both seemed to be protective against breast cancer, regardless of menopausal status or BMI. (Cancer Epidemiol Biomarkers Prev 2008;17(12):3396–401)

Friday, December 26, 2008

Nanoparticles Penetrate the Intact Skin, Greater Penetration of Damaged Skin

BrooklynDodger(s) comment: Currently a prominent use of nanoparticles is nano sized titanium dioxide (an IARC 2B carcinogen) in skin treatments. Another post noted that these titanium dioxide particles could penetrate the olfactory epithelium and find there way the brain. Here's a study of silver nanoparticles (does anyone know what they might be used for?) penetrating the regular skin in a laboratory study.

This study should be considered hazard identification - at least as far as exposure goes. The next step in the NAS paradigm is dose-response assessment. We need more than two points - intact and damaged - and more than a single application in a laboratory system.

ToxicologyVolume 255, Issues 1-2, 8 January 2009, Pages 33-37

Human skin penetration of silver nanoparticles through intact and damaged skin

Francesca Filon Laresea, , , Flavia D’Agostina, Matteo Croserab, Gianpiero Adamib, Nadia Renzic, Massimo Bovenzia and Giovanni Mainad
"There is a growing interest on nanoparticle safety for topical use. The benefits of nanoparticles have been shown in several scientific fields, but little is known about their potential to penetrate the skin. This study aims at evaluating in vitro skin penetration of silver nanoparticles. Experiments were performed using the Franz diffusion cell method with intact and damaged human skin. Physiological solution was used as receiving phase and 70 μg/cm2 of silver nanoparticles coated with polyvinylpirrolidone dispersed in synthetic sweat were applied as donor phase to the outer surface of the skin for 24 h. The receptor fluid measurements were performed by electro thermal atomic absorption spectroscopy (ETAAS). Human skin penetration was also determined by using transmission electron microscope (TEM) to verify the location of silver nanoparticles in exposed membranes.
Median silver concentrations of 0.46 ng cm−2 (range Our experimental data showed that silver nanoparticles absorption through intact and damaged skin was very low but detectable, and that in case of damaged skin it was possible an increasing permeation of silver applied as nanoparticles. Moreover, silver nanoparticles could be detected in the stratum corneum and the outermost surface of the epidermis by electron microscopy.
We demonstrated for the first time that silver applied as nanoparticles coated with polyvinylpirrolidone is able to permeate the damaged skin in an in vitro diffusion cell system

Thursday, December 25, 2008

Nuclear Safety and Risk Assessment

BrooklynDodger(s) comments: As pressure mounts for new expansion of nuclear power, the risk assessment battle will resume. The canonical example of public "misperception" of risk is the often published table comparing risk from a nuclear accident to the risk from driving to the grocery store. For the purpose of this blog posting, the Dodger(s) won't address the overall topic.
However, this press account reminds us that any industrial process has all sorts of unanticipated ways it can go wrong... can go wrong... can go wrong....

Nuclear safety left hanging as crane dangled fuel rods
Michigan incident got warning but no fine

March 18, 2006

"A 110-ton load of nuclear waste dangled for 55 hours above a cooling pool last October as two workers at a southwest Michigan nuclear power plant improperly manipulated a crane that had frozen, federal regulators concluded in a recent review of the incident

"...Under the NRC's worst-case scenario, if the suspended load had accidentally dropped, a fire could have ignited, leading to formation of a radioactive cloud. The cloud could have put thousands of people downwind of the plant -- all the way to Kalamazoo -- at risk of fatal radiation poisoning....

The scariest nuclear accident in Michigan was the 1966 partial meltdown of the Fermi 1 nuclear reactor near Monroe that inspired the 1975 book "We Almost Lost Detroit."...
Plant officials maintained that only 1% of the uranium fuel melted, but critics say the plant came close to a runaway reaction that could have killed people for miles around the plant.
No radiation was released, but the plant never returned to useful operation."

Human Ecology in a Declining Economy

BrooklynDodger(s) comment: Sometimes the source is not peer reviewed; this comes from the Detroit Free Press which is almost underwater like the car companies. The Dodger(s) has(have) seen coyotes in riverside Detroit (not the business district, but habited.) The near, or maybe total collapse of the Detroit auto industry exemplifies Chaos theory - moderate to small changes in an adverse direction may be recovered from, but a little push may crash the whole system. The system includes people living nearby the companies and their factories. Chaos also says that once a system crashes, it may never come back to where it was.

This applies to the wildlife around Detroit. Those who said let the companies fail suggest we live in a "dog eat dog" world. There's something else that eats dogs, in this case, coyotes.

The Dodger(s) didn't have time to compare sitesfor this, and, embarrassed by the notion of posting a wikipedia link, provide the following lecture notes

Coyotes clash with humans, small pets in Detroit suburbs
Trapping, shooting considered


"Kim Sikand had seen coyotes in her Bloomfield Hills yard, and she had heard city advice to keep pets under watch...

Tuesday, December 23, 2008

Diethanolamine Inhibits Brain Development When Applied to the Skin

Brooklyn Dodger(s) comments: DEA ought to be a 2B carcinogen, by skin application, although it's not, for reasons to be discussed in another post. The Dodger(s) interest in DEA relates to its presence in MWF's. But the heat around DEA which fuels mechanistic research is generated by the presence of DEA as an unwanted impurity in skin lotion. One theory is that liver damage and liver cancer in mice follow from choline depletion. Here we have an investigation of developmental disability from DEA applied to the skin.

The effect level in this study is 80 mg/kg/day for 10 days, with 60 mg/kg as a NOEL. The Dodger(s) will context this with the NTP bioassay in another post. So the uncertainty factors of 10 for acute to chronic, 10 for animal to human, and 10 for population variability would generate a RfD of 60 ug/kg/day as a default. [But, is 10 days acute or chronic? the fetus is sensitive for only 10 days or maybe only 1 day within the 10. but there's an effect at 60 mg/kg, just not significant. so maybe the real NOEL is 40]

Now comes a skin lotion, with 1.8 ppm DEA, likely an impurity in a diethanolamide-fatty acid condensate. [Still dirty after all these years?]. The 3 women dosed had plasma levels varying by 3-fold from top to bottom, with 5 nmoles/ml about the mean, compared to 1250 in the 80 mg/kg mice. A ratio of about 250 from the effect level. The Dodger(s) think this is too close.

Hazcomers take note.


Dose Response Effects of Dermally applied Diethanolamine on Neurogenesis in Fetal Mouse Hippocampus and Potential Exposure of Humans

Corneliu N. Craciunescu, Mihai D. Niculescu, Zhong Guo, Amy R. Johnson, Leslie Fischer, and Steven H. Zeisel

Toxicol. Sci. 2009 107: 220-226;

"Diethanolamine (DEA) is a common ingredient of personal care products. Dermal administration of DEA diminishes hepatic stores of the essential nutrient choline and alters brain development. We previously reported that 80 mg/kg/day of DEA during pregnancy in mice reduced neurogenesis and increased apoptosis in the fetal hippocampus. ... Timed-pregnant C57BL/6 mouse dams were dosed dermally from gestation day 7–17 with DEA at 0 (controls), 5, 40, 60, and 80 mg/kg body/day. Fetuses (embryonic day 17 [E17]) from dams treated dermally with 80 mg/kg body/day DEA had decreased neural progenitor cell mitosis at the ventricular surface of the ventricular zone ... Also, this dose of DEA to dams increased rates of apoptosis in E17 fetal hippocampus ... This dose of DEA resulted in accumulation of DEA and its metabolites in liver and in plasma. At doses of DEA less than 80 mg/kg body/day to dams, there were no differences between treated and control groups. In a small group of human subjects, dermal treatment for 1 month with a commercially available skin lotion containing 1.8 mg DEA per gram resulted in detectable plasma concentrations of DEA and dimethyldiethanolamine, [BrooklynDodger(s) comment: risk assessment conclusion implied but not justified] but these were far below those concentrations associated with perturbed brain development in the mouse."

Monday, December 22, 2008

Diesel Particulate - What Part of Probably Carcinogenic Don't You Understand?

BrooklynDodger(s) Comments: Diesel particulate matter is an IARC 2A carcinogen because there is "sufficient" evidence in laboratory studies, but human studies were considered "limited" by the last working group to take it up, in 1989. Despite multiple studies among truck drivers and railroad personnel showing increased lung cancer, including some controlling for smoking, it wasn't enough to pull the trigger on "known." With some justice, it can be argued that there's lots of other junk in the air on the road, gasoline engine exhaust if possibly carcinogenic, there's some evidence for particulate air pollution being associated with increased community cancer. Attributing the excess cancer only to diesel can be criticized.

The study quoted here strengthens the evidence in people, but the wording points to an intermediate step. IARC evaluates "exposure circumstances," and mixtures in addition to particular agents. Maybe a step to consensus is to evaluate the exposure circumstance of truck driving or exposure to vehicle exhaust - evidence for carcinogenicity of these exposures ought to be sufficient.

Emissions from compressed natural gas engines should be bioassayed. Lighter in weight than diesel, but many nanoparticles.

Environ Health Perspect. 2008 October; 116(10): 1327–1332.

Lung Cancer and Vehicle Exhaust in Trucking Industry Workers

Eric Garshick,1,2 Francine Laden,2,3,4 Jaime E. Hart,2,3 Bernard Rosner,2 Mary E. Davis,3,5 Ellen A. Eisen,6,7 and Thomas J. Smith3

src="" border=0>Abstract

"Background. An elevated risk of lung cancer in truck drivers has been attributed to diesel exhaust exposure. Interpretation of these studies specifically implicating diesel exhaust as a carcinogen has been limited because of limited exposure measurements and lack of work records relating job title to exposure-related job duties.
Objectives. We established a large retrospective cohort of trucking company workers to assess the association of lung cancer mortality and measures of vehicle exhaust exposure.
Methods. Work records were obtained for 31,135 male workers employed in the unionized U.S. trucking industry in 1985. We assessed lung cancer mortality through 2000 using the National Death Index, and we used an industrial hygiene review and current exposure measurements to identify jobs associated with current and historical use of diesel-, gas-, and propane-powered vehicles. We indirectly adjusted for cigarette smoking based on an industry survey.
Results. Adjusting for age and a healthy-worker survivor effect, lung cancer hazard ratios were elevated in workers with jobs associated with regular exposure to vehicle exhaust. Mortality risk increased linearly with years of employment and was similar across job categories despite different current and historical patterns of exhaust-related particulate matter from diesel trucks, city and highway traffic, and loading dock operations. Smoking behavior did not explain variations in lung cancer risk.
Conclusions. Trucking industry workers who have had regular exposure to vehicle exhaust from diesel and other types of vehicles on highways, city streets, and loading docks have an elevated risk of lung cancer with increasing years of work."

Sunday, December 21, 2008

Presence of Diethanolamine in currently used MWF confirmed, skin penetration observed to be predominant mode of exposure.

BrooklynDodger(s) comment: Finnish investigators compared the potential for skin absorption to that of ethanolamine aerosol in machine shops. The first finding was that diethanolamine (DEA) was present in the fluids. [NTP found clear evidence that diethanolamine causes liver cancer and liver disease in mice when applied to the skin. NIOSH found that an MWF caused liver pathology in mice when applied to the skin, likely from DEA content.] The investigators state that 100 times as much DEA was on the skin compared to that inhaled. There is no good quantitative way to estimate historical exposure to ethanolamines by skin absorption in MWF operation. A case of liver disease in a worker exposed to MWF may be due to DEA skin absorption, even if air levels are very low.


Determination of Occupational Exposure to Alkanolamines in Metal-Working Fluids.

Annals of Occupational Hygiene. 51(2):153-160, March 2007.

Henriks-Eckerman, Maj-Len 1,*; Suuronen, Katri 2; Jolanki, Riitta 2; Riala, Riitta 2; Tuomi, Timo 2

Abstract: Overall exposure to alkanolamines in metal-working fluids (MWFs) in machine shops was studied by determining alkanolamines in air samples and in rinse-off samples from the hands of machinists. Methods for collecting airborne alkanolamines and alkanolamines absorbed to the skin of the hands were developed and tested. The exposure measurements were carried out in nine machine shops. After a 2 h working period the dominant hand of 37 machinists was rinsed with 200 ml of 20% isopropanol for 1 min in a plastic bag. Personal air samples were also collected during the 2 h working period onto acid-treated glass fibre filters. The filter samples were desorbed with methanol and analysed by liquid chromatography with mass spectrometric detection (LC-MS). The rinse-off samples were also analysed for alkanolamines by LC-MS. The median air concentration of monoethanolamine (EA) was 57 [mu]g m-3, diethanolamine (DEA) 64 [mu]g m-3 and triethanolamine (TEA) 6 [mu]g m-3. The workers' overall exposure to alkanolamines was estimated by calculating the amount in inhaled air and the amount on the skin. The median amount of EA on the skin of the dominant hand was 9-43 times the median amount in inhaled air during 2 h exposure. The corresponding ratio for DEA was 100 and for TEA 170. According to this study the exposure to alkanolamines occurs mainly through the skin. EA was the only alkanolamine with a noticeable inhalation uptake compared to the skin uptake. Total exposure to MWFs may be reduced by reducing skin exposure. The hand rinsing method can be used to assess the efficiency of protective gloves.

Saturday, December 20, 2008

Internet Research Proves the Dodger(s) Wrong 48

BrooklynDodger(s) Comment: The Dodger(s) bought a replica jersey with a script "Brooklyn" rather than "Dodgers." The Dodger(s) searched the net for pictures of such a jersey, couldn't find one, and then opined (more than once and in public) that there was no such thing and that the jersey was a sign of fraud, falsification and other frippery and drippery on behalf of the hated Los Angeles Dodgers. (This did not prevent the Dodger(s) from sometimes wearing the jersey, since it gave an opportunity to denounce Walter O'Malley again.)

Crow is being served tonight for dinner. Following the above link will take you to a picture of the 1940 Dodgers, with "Brooklyn" scripted on their jerseys. Note the racial composition of the team.

Friday, December 19, 2008

Speculating on Mode of Action for Styrene Carcinogenicity - Is Houdini in the Wings?

BrooklynDodger(s) comment: Styrene is one of those old, huge-use carcinogens which has gotten lost in the regulatory forest. Styrene is used in open-to-the-workroom air processes making fiberglass reinforced articles like boats and bathtubs. It's sprayed. The OSHA PEL is 100 ppm, and is not on very many lists for an update from 1968. The TLV is 20 ppm, obviously better but not set based on a disciplined process. The EPA reference concentration is 1 mg/m^3 (not ppm) based on CNS effects, set in 1993.

The classification of styrene as a 2A carcinogen in 2002 is explained in an IARC monograph, now available in full text.

What's up with styrene in the risk assessment "community" is the mouse Clara cell hypothesis. Clara cells (the Dodger(s) think) are the lung's version of the Kuppfer cell - a resident phagocytic cell in the parenchema of the tissue. [It's more complicated than this.]

Several lower molecular weight vapors cause lung tumors in mice, but not rats. Of these, several cause liver tumors in both species. So one approach to making the risk estimate lower is to parallogramate mouse, rat and human clara cell properties. This study finds increased levels of a protein the Dodger(s) never heard of before, and messinger RNA for that protein (a technique unknown in the Dodger(s) youth), following a single dose. We can expect a similar study in rats, and then an argument that for styrene, people are rats, not mice. So don't worry, be happy.

[Remember, this ain't the NAS, it's just blogging. The Dodger(s) disclaimer on being wrong and flippant.]

Toxicology Letters Volume 183, Issues 1-3, 15 December 2008, Pages 28-35

CC10 mRNA and protein expression in Clara cells of CD-1 mice following exposure to styrene or its metabolites styrene oxide or 4-vinylphenol

Jill A. Harvilchucka, Rebekah J. Zurbrugga and Gary P. Carlson, a,
aSchool of Health Sciences, Purdue University, 550 Stadium Mall Drive, West Lafayette, IN 47907-2051, United States

"Styrene, widely used in manufacturing, has both acute and chronic effects in humans. In mice, styrene is both hepato- and pneumo-toxic and causes lung tumors. The primary site for styrene metabolism and its effects in mouse lung is the Clara cell, ...The mode of action for styrene-induced lung tumor formation has yet to be elicited, yet one possibility relates to oxidative stress ...

[single dose intraperitoneal injection]...

[lots of changes in biochemical markers] ...

These studies demonstrate that acute changes in lung CC10 protein and mRNA expression do occur following in vivo treatment with styrene and its metabolites. These changes may be early indicators for a potential mechanism for lung tumor formation in mice as it relates to oxidative stress and the possibility deserves further study.

Thursday, December 18, 2008

Injury Control in the more American part of America

Am J Prev Med Volume 36, Issue 1, Pages 49-55 (January 2009)

Rural–Urban Differences in Injury Hospitalizations in the U.S., 2004

Jeffrey H. Coben, MDabc, Hope M. Tiesman, PhDbc, Robert M. Bossarte, PhDbc, Paul M. Furbee, MAc

Despite prior research demonstrating higher injury-mortality rates among rural populations, few studies have examined the differences in nonfatal injury risk between rural and urban populations. The objective of this study was to compare injury-hospitalization rates between rural and urban populations using population-based national estimates derived from patient-encounter data.
A cross-sectional analysis of the 2004 Nationwide Inpatient Sample was conducted in 2007. Rural–urban classifications were determined based on residence. SUDAAN software and U.S. Census population estimates were used to calculate nationally representative injury-hospitalization rates. Injury rates between rural and urban categories were compared with rate ratios and 95% CIs.
An estimated 1.9 million (95% CI=1,800,250–1,997,801) injury-related hospitalizations were identified. Overall, injury-hospitalization rates generally increased with increasing rurality; rates were 27% higher in large rural counties (95% CI=10%, 44%) and 35% higher in small rural counties (95% CI=16%, 55%). While hospitalization rates for assaults were highest in large urban counties, the rates for unintentional injuries from motor vehicle traffic, falls, and poisonings were higher in rural populations. Rates for self-inflicted injuries from poisonings, cuttings, and firearms were higher in rural counties. The total estimated hospital charges for injuries were more than $50 billion. On a per-capita basis, hospital charges were highest for rural populations.
These findings highlight the substantial burden imposed by injury on the U.S. population and the significantly increased risk for those residing in rural locations. Prevention and intervention efforts in rural areas should be expanded and should focus on risk factors unique to these populations."

Wednesday, December 17, 2008

Lifestyle Prevention of Cancer: Anorexia and Teenage Pregnancy

Caloric Restriction and Incidence of Breast Cancer

Karin B. Michels, ScD, MSc, MPH; Anders Ekbom, MD, PhD
JAMA. 2004;291:1226-1230.

Context Restricting caloric intake is one of the most effective ways to extend lifespan and to reduce spontaneous tumor occurrence in experimental animals, but whether similar associations hold in humans has not been appropriately studied.
Objective To determine whether caloric restriction in early life reduces the risk of invasive breast cancer.
Design, Setting, and Participants Retrospective cohort study using data from the Swedish Inpatient Registry, the Swedish Cancer Registry, the Swedish Death Registry, and the Swedish Fertility Registry. Participants were 7303 Swedish women hospitalized for anorexia nervosa prior to age 40 years between 1965 and 1998. Women were excluded (n = 31) if they were diagnosed with cancer prior to their first discharge from hospitalization for anorexia nervosa.
Main Outcome Measure Incidence of invasive breast cancer.
Results Compared with the Swedish general population, women hospitalized for anorexia nervosa prior to age 40 years had a 53% (95% confidence interval [CI], 3%-81%) lower incidence of breast cancer; nulliparous women with anorexia nervosa had a 23% (95% CI, 79% higher to 75% lower) lower incidence, and parous women with anorexia nervosa had a 76% (95% CI, 13%-97%) lower incidence.
Conlusions Severe caloric restriction in humans may confer protection from invasive breast cancer. Low caloric intake prior to first birth followed by a subsequent pregnancy appears to be associated with an even more pronounced reduction in risk

BrooklynDodger(s) comment: Forgive this comment for snarkyness. The Dodger(s) twitch when authorities advocate decreasing disease risk, in this case breast cancer, through "healthy" individual life choices. The other side of that coin is blaming the victim for not making those choices. This framework is rife in the mainstream cancer prevention literature (for example, Cancer Facts from the ACS]: do what your mother told you, eat your vegatables, exercise, don't smoke [the Dodger(s) agree with this, although cancer risks from cigarettes are overestimated, the subject of another post], drink or eat fried food.

The observation of this report is that anorexia, to the point of hospitalization, is associated with up to a 75% reduced risk of breast cancer. The Dodger(s) remember, but couldn't retrieve, a report with a similar result for anorexia combined with teenage pregnancy.

So, to prevent breast cancer, promote anorexia [and maybe other risk behavior] among your daughters.

Contradicting this advice, the Dodger(s) note(s) that persons in the lowest decile of BMI suffer increased mortality from all causes compared to persons who are classified as "overweight" by BMI.

Remember, this ain't the NAS, it's only blogging.

Tuesday, December 16, 2008

Get the Lead Out, Evidence That OSHA's Lead Standard Lets Workers Get Sick

Occurrence of lead-related symptoms below the current occupational safety and health act allowable blood lead levels.

J Occup Environ Med - 01-MAY-2003; 45(5): 546-55
Rosenman KD; Sims A; Luo Z; Gardiner J

To determine the occurrence of symptoms of lead toxicity at levels below the current allowable Occupational Safety and Health Act blood lead level of 50 micrograms/dL, standardized telephone interviews were conducted of individuals reported to a statewide laboratory-based surveillance system. Four hundred and ninety-seven, or 75%, of the eligible participants were interviewed. Gastrointestinal, musculoskeletal, and nervous system symptoms increased with increasing blood lead levels. Nervous, gastrointestinal, and musculoskeletal symptoms all began to be increased in individuals with blood leads between 30-39 micrograms/dL and possibly at levels as low as 25-30 micrograms/dL for nervous system symptoms. The results of this study of increased symptoms are consistent with and provide added weight to previous results showing subclinical changes in the neurologic and renal systems and sperm counts at blood lead levels currently allowed by the Occupational Safety and Health Act.


BrooklynDodger(s) comments: The current level of concern for lead-in-blood in children, and by extension pregnant women, is 10 ug/100g. Little thought has been given to a level of concern in already born and grown up workers.

From the lead poisoning epidemics associated with tetraethyl lead and lead body solder, both auto industry outbreaks of the '20's and '30's, came the notion of controlling lead toxicity by monitoring body burden and removing workers from exposure. Hopefully something would have been done about the exposures, but mostly the response was yo-yo ing the employee.

The OSHA lead standard was promulgated in 1976, based on the science available a few years before. At that time, lead in blood of 80 ug/100g was the informal criterion for removal, although values up to 100 were observed. Most workers in lead industries has lead in blood over 40. OSHA dropped the removal trigger to 60 for a single test or a 3 test moving average of 50, with return permitted at 40. Levels of 40 were routinely observed in the general population not exposed occupationally.

Science had accumulated between 1975 and 1993, when the OSHA construction lead standard was promulgated. [Construction was omitted from 1910.1025; the extension of those protections to construction was required by legislation aimed at residential lead abatement.] Despite new data, the 60/50/40 regime was left in place.

This report from a state lead surveillance program reveals that symptoms of lead intoxication arise at 30 ug and maybe as low as 20 ug in adult workers.

The OSHA lead-in-air limit remains the strictest in the world. The Dodger(s) has(have) not surveyed medical removal levels for occupational exposures around the world.

But, the take home lesson is that one of OSHA's most protective chemical exposure standards permits exposures which cause frank symptoms among workers.

Monday, December 15, 2008

Social Epidemiology

BrooklynDodger(s) comments: Those of us on the chemical exposure side of public health tend to be weak on social epidemiology. Beyond the "healthy worker effect" we don't think about the impact of social environment on health very much.

The healthy worker effect is likely partially an artifact for short duration of observation, but it also reflects the association between improved social class and improved health and reduced mortality. Educational level may reflect improved social class, independent of income although confounded with income. This Israeli study indicates that higher education in your spouse improves your mortality experience.

[The Dodger(s) confess not to have read the full text, and to have found some of the abstract confusing.]

Social Science & MedicineVolume 62, Issue 8, April 2006, Pages 2014-2023

Effects of husbands’ and wives’ education on each other's mortality

Dena H. Jaffe, , Zvi Eisenbach, Yehuda D. Neumark and Orly Manor

"We found that the educational attainment of both spouses were significant predictors of one's own overall mortality. For CVD mortality, however, a wife's educational attainment was a stronger predictor of her husband's risk of dying than his own educational level, while for women a husband's education had little affect. Educational discrepancy between partners did not affect overall mortality ... highly educated women had an almost two-fold increased risk of CVD mortality when married to less educated husbands, while lesser-educated women were not affected by their spouses’ educational attainment."

Sunday, December 14, 2008

It's Just Blogging

BrooklynDodger(s) Comment: So, here's a disclaimer, in case someone eventually discovers who the BrooklynDodger(s) is(are). Blogging is supposed to be quick (symbolized by the illustration) and conversational comments on items found in the media. Just because the Dodger(s) comment on here are frequently from weighty journals, it doesn't change the "quick and conversational" part. Sometimes the Dodger(s)' comments may be incorrect because of lack of searching literature to confirm. The Dodger(s) may have only read the abstract rather than the full text. The Dodger(s) may make snarky comments (without adding "Just Kidding."

Just remember, this ain't the National Academies, it's just blogging.

Saturday, December 13, 2008

What's Up With "BrooklynDodger(s)"?

BrooklynDodger(s) comment: The premier public health blog is Effect Measure. Anyone reading this blog surely reads that. The authors of Effect Measure say they are plural and cognomenize themselves as the Reveres and gender identify by adding a "Mrs. Revere" to their narrative.

[Yes, the Dodger(s) had to look up the spelling and confirm the definition: Cognomen is "A name, especially a descriptive nickname or epithet acquired through usage over a period of time."]

So the Dodger(s) [formerly the Dodger] invoke the ambiguity of number and gender, at the cost of a pronoun. And, the Dodger(s) further note that "Brooklyn" may be a state of mind, not a place, and that the team formerly known as the Brooklyn Dodgers has now played more games in Los Angeles than in Brooklyn.

Friday, December 12, 2008

Nanoparticle Titanium Dioxide Hazards Identified

BrooklynDodger(s) Comment: Someday, the continuing myth that little to nothing is known about the hazards of nanoparticles or nanotechnology will be busted. ( The Dodgers(s) have previously noted that Titatanium Dioxide of all sizes is an IARC 2B carcinogen, with little controversy about nano sized. TiO2 used to be a negative control, supposedly inert and non-toxic material before it turned out to be a carcinogen. TiO2 is one of two major use nanotechnology materials, the other being carbon nanotubes.

This publication comes from a Chinese institution, a notice that development in China also includes scientific capabilities. So our colleagues from China have shown that intra nasal TiO2 gets into the brain and causes visible lesions. Nasal instillation is a valid route for hazard identification, and with some modeling could be a valid route for dose response assessment. However, for now, the warning for those who use TiO2 based skin creams, a major use, is to wash your hands before picking your nose.

Toxicology LettersVolume 183, Issues 1-3, 15 December 2008, Pages 72-80

Potential neurological lesion after nasal instillation of TiO2 nanoparticles in the anatase and rutile crystal phases

Jiangxue Wanga, b, Chunying Chena...

Laboratory for Bio-Environmental Effects of Nanomaterials and Nanosafety and Key Lab of Nuclear Analytical Techniques, Institute of High Energy Physics, Chinese Academy of Sciences, Beijing 100049, PR China

"Nanoscale titanium dioxide (TiO2) is massively produced and widely used in living environment, which hence make the potential risk to human health. ...Central nervous system (CNS) is the potential susceptible target of inhaled nanoparticles, ...We report the accumulation and toxicity results in vivo of two crystalline phases of TiO2 nanoparticles (80 nm, rutile and 155 nm, anatase; purity >99%). The female mice were intranasally instilled with ...TiO2 nanoparticles suspension every other day for 30 days. ...The obvious morphological changes of hippocampal neurons and increased GFAP-positive astrocytes in the CA4 region were observed, which were in good agreements with higher Ti contents in the hippocampus region. Oxidative stress occurred obviously in whole brain of exposed mice ... To summarize, results provided the preliminary evidence that nasal instilled TiO2 nanoparticles could be translocated into the central nervous system and cause potential lesion of brain, and the hippocampus would be the main target within brain."

Magnetic fields and Cardiovascular Disease

The burden of attempting daily posting is already weighing on the Dodger(s), hence this reference to a study of an exposure about which the Dodger(s) know little.

This marks an early appearance of a 2009 publication.

The bottom line about EMF and adverse health effects is that human studies are equivocal, meaning not completely null. This study presents an additional null result. However, at best, epidemiology rules out an excess greater than 50% above the control rate, for hazard identification purposes.

This report is a secondary data analysis based on linkage of a job exposure matrix with a sample of U.S. workers from the National Longitudinal Mortality Study (have to search for this data base). The Dodger(s) also have to persue the exposure matrix.

Bowman JD, Touchstone JA, Yost MG. A population-based job exposure
matrix for power-frequency magnetic fields. J Occup Environ Hyg. 2007;

Population-Based Cohort Study of Occupational Exposure to Magnetic Fields and Cardiovascular Disease Mortality

Annals of EpidemiologyVolume 19, Issue 1, January 2009, Pages 42-48

Anna R. Cooper, Edwin Van Wijngaarden, Susan G. Fisher, M. Jacob Adams, Michael G. Yost, Joseph D. Bowman

"After adjustment for demographic factors, there were no significant excess risks between individuals with medium (0.15 to <0.20 μT), high (0.20 to <0.30 μT), or very high (≥0.30 μT) exposure levels as compared with individuals with background exposure levels of MF (<0.15 μT) for the CVD mortality outcomes. Indirect adjustment for potential confounding by current smoking prevalence did not change the pattern of these results."

Thursday, December 11, 2008

Hazardous Chemical Exposures Near Schools

[A new funding source for Johns Hopkins - USA Today. Maybe in future Bloomberg News will fund the Bloomberg School of Public Health.]

The reported study was directed at toxic heavy metals and volatile organic chemicals. Levels were found at some schools, above, the Dodger(s) presume, EPA RfC's or ATSDR MRL's. This sampling campaign might have been more productive had it focused on PM2.5 or Diesel Particulate Matter (DPM) as measured by elemental carbon. Both PM2.5 and DPM pose far more clear and present dangers at prevailing levels in the street than the contaminants reported at the levels detected.
Air tests reveal elevated levels of toxics around schools

\By Brad Heath and Blake Morrison, USA TODAY
MIDLAND, Pa. — In this borough of 2,900 in the westernmost part of the state, the steel industry used to be the primary employer. Today, Midland's schools offer the most jobs — and now are beginning to unravel a mystery that could affect the health of their students.

Brooklyn Dodger Comes Back from the Bench

After hiatus, Brooklyn Dodger(s) has (have) resumed motivation to post, and conquered the various changes in Blogger to start again.