PART part II

The program assessment rating tool (PART) results of Labor Department programs by OMB are shown on the President’s Budget page.

The PART is a mechanism to withdraw funding from programs. It’s a No Child Left Behind [that is, No School Left Unpunished] approach to government service.

It’s a bad guy idea, for sure, like quantitative risk assessment. While we were right to fight QRA, smart people have since found that QRA actually supported very strict standards for chemicals for which there is an adequate data set, at least in the occupational environment. [The Bad Guys figured that out as well, and have since launched a campaign against QRA called Houdini Risk Assessment, which aims to make the hazard identification step disappear.]

BrooklynDodger fears that PART will survive beyond this administration. So we public health people have to address the PART and see if it can be turned in a positive direction.

The Dodger was defeated in abstracting the OSHA entry for PART. One extract is below. Read it and weep, but don’t mourn.

All DOL:


TABLE OF CONTENTS
Rating Page
Black Lung Benefits Program............................................................................. Moderately Effective.................. 3
Bureau of Labor Statistics.................................................................................. Effective...................................... 16
Community Service Employment for Older Americans.................................... Ineffective................................... 26
Davis-Bacon Wage Determination Program...................................................... Results Not Demonstrated......... 34
Dislocated Worker Assistance............................................................................. Adequate..................................... 49
Employee Benefits Security Administration (EBSA)........................................ Moderately Effective.................. 61
Employment Service............................................................................................ Adequate..................................... 73
Federal Employees Compensation Act (FECA)..................................................Moderately Effective.................. 88
H-1BLabor Applications Program...................................................................... Moderately Effective................ 98
International Child Labor Program and Office of Foreign Relations............... Adequate..................................... 109
Job Corps.............................................................................................................. Moderately Effective.................. 120
Migrant and Seasonal Farmworkers.................................................................. Ineffective................................... 134
Mine Safety and Health Administration............................................................ Adequate..................................... 146
Native American Programs - Workforce Investment Act................................. Adequate..................................... 158
Occupational Safety and Health Administration...............................................Adequate..................................... 174
Office of Federal Contract Compliance Programs (OFCCP)............................. Adequate..................................... 184
Pensions Benefit Guaranty Corporation............................................................ Moderately Effective.................. 197
Permanent Labor Certificate Program............................................................... Adequate..................................... 210
Trade Adjustment Assistance............................................................................. Ineffective................................... 221
Unemployment Insurance Administration State Grants.................................. Moderately Effective.................. 231
Youth Activities................................................................................................... Ineffective................................... 243

One of OSHA's bad marks:

2.REG1 Are all regulations issued by the program/agency necessary to meet the stated goals of the
program, and do all regulations clearly indicate how the rules contribute to achievement
of the goals? NO
Many OSHA regulations (e.g., OSHA's permissible exposure limits, which were promulgated in the 1970s) are in need of updating/streamlining. OSHA's current Standards Improvement Project, which entails the review of rules to update and simplify requirements, is a step in the right direction but should go further. In April 2002 OSHA asked numerous consensus standard organizations for their priorities for updating OSHA standards based on their requirements. OSHA is reviewing the feedback it received to determine appropriate next steps. OSHA's regulations show a fairly clear relationship to OSHA's strategic goals.

OSHA Standards Improvement Project Phase I, 62 FR 40141; Longshoring Standard Improvement Project, 63 FR 33450; OSHA Standards Improvement Project Phase II is scheduled to be published in October 2002. 12%

Gene Silencing - Genotoxicity without Mutations

Another high powered mechanistic approach to chemical carcinogenesis – “Gene Silencing” - needs interpreting within the environmental paradigm. The risk assessment issue is whether mechanism suggests that directly observable carcinogenic effects, of necessity in a high dose range, persist to low dose ranges. Low dose continuity is generally accepted for “genotoxic” carcinogens – mutagenicity positive materials. Now comes “gene silencing” – an epigenetic event, but heritable.

Virtually all mutations make the gene product less effective. Mutational events cause cancer by disabling genes which make proteins or other products which prevent uncontrolled cellular growth.

The mutagenicity bioassay doesn’t target these specific genes. Instead, it takes a bacteria strain mutated to be unable to grow in a particular medium because of a disabled gene, and machine guns the genome to produce a few reverse mutants with the gene restored. Colonies growing indicate mutagenic potential of the agent, and thus somatic mutation potential.

Gene silencing chemicals would be invisible in this system.

Effectively, non-genotoxic agents should act just like genotoxic agents, advancing a step to producing a clone of uncontrolled cells which may progress to a tumor.

Carcinogenesis vol.26 no.9 pp.1481--1487, 2005

COMMENTARY
Silencing of genes by promoter hypermethylation: key event in
rodent and human lung cancer
Steven A.Belinsky1
Lung Cancer Program, Lovelace Respiratory Research Institute,
2425 Ridgecrest Drive SE, Albuquerque, NM 87108, USA
1Email: sbelinsk@LRRI.org

Transcriptional silencing by CpG island hypermethylation has become a critical component in the initiation and progression of lung cancer. The ability of pharmacologic agents to reverse promoter hypermethylation also makes it an attractive target to pursue for prevention of lung cancer. Animal models, together with studies in humans have fostered significant advances in elucidating the role of gene-specific methylation in cancer initiation and progression, the modulation of promoter methylation by carcinogen exposure and the ability to block tumor development by preventing epigenetically mediated gene silencing. These advances represent the beginning of efforts to develop a progression model for lung cancer that should aid efforts for early detection and gene targeting for therapy, and the development of preventive interventions that reverse epigenetic-mediated gene silencing.

PART I: Wasting away in MBA ville

BrooklynDodger recently learned of PART – the Program Assessment Review Tool. It’s an OMB idea, which would generally justify cutting budgets. The Dodger will comment more in future, but here is the account of the process from the 2004 budget.

Most government programs have stated goals and some covert goals. For instance, the covert goal of the military is that the US rules the world. Here, OMB forces agencies to convert these goals into a numerical form, then uses that number to beat the agency into submission. It’s MBO. But in corporate MBO, the managers of the process and the subordinates both share a stated goal of making money by a product or delivering a service. In the PART environment, the managers of the process are hostile to government outside the military and Homeland Security.

NIOSH, OSHA and MSHA are currently struggling to improve their rating from adequate, putting them above the line were half of government programs were rated “results not demonstrated,” and 5% rated “ineffective.”

…the Administration plans to review approximately one-fifth of all federal programs every year, so that by the 2008 budget submission every program will have been evaluated using this tool. For this year, OMB completed reviews for 234 diverse programs as a representative sample of government programs, as well as to test the flexibility of the PART. Chosen programs vary by type (such as regulatory, grants, or direct assistance), as well as size. To test how well the PART would confirm expectations, some programs generally considered effective (such as the National Weather Service) were included, as well as some widely criticized as less effective, (such as compliance with the Earned Income Tax Credit (EITC)). Finally, several items of great interest to the President or the Congress were selected, such as programs scheduled for reauthorization this year.

The PART’s approximately 30 questions (the number varies depending on the type of program being evaluated) ask for information which responsible federal managers should be able to provide. For instance:

• Is the program designed to have a significant impact in addressing the intended interest, problem,or need?
• Are federal managers and program partners (grantees, sub-grantees, contractors, etc.) held
accountable for cost, schedule, and performance results?
• Has the program taken meaningful steps to address its management deficiencies?
• Does the program have a limited number of specific, ambitious long-term performance goals that focus on outcomes and meaningfully reflect the purpose of the program?
• Does the program (including program partners) achieve its annual performance goals?

The burden is on the program to demonstrate performance. Absent solid evidence to support a positive answer, the answer is deemed not favorable and the program receives a lower rating. The requirement of hard evidence fulfills the principle that federal managers must be held accountable for proving their programs are well designed and well managed.

Programs must also prove they are working. Programs that cannot demonstrate they are achieving results either because they have failed to establish adequate performance measures, or have no supportive performance data show a rating of Results Not Demonstrated. The other ratings are, in descending order: Effective, Moderately Effective, Adequate, and Ineffective. For more information on how the PART is used see the sidebar entitled “How the PART Works” in this chapter. Even greater detail is provided in the Performance and Management Assessments volume.

Nanotoxicology backs Macrohype of Nanoparticles

BrooklynDodger was attracted to this abstract because of wonder whether nanotoxicology is macrohype. The Dodger has already renamed fine particle health effects nanoparticle research.  Brooklyndodger skimmed the abstract and questioned, how do these indeces of toxicity compare to known particle toxicants?  The full text of the paper actually answers these questions; none of this very important data made the abstract.  [Reviewers’ and editors’ benign neglect?]

In parallel experiments, rats got 2 mg/rat of ultrafine carbon black and chrysotile asbestos, compared to the 0.5-2 mg/rat of ground and unground nanotubes. The investigators noted that “CB had a specific surface area of 66.8 m2/g,” an interesting number for which the Dodger has no comparison. The Dodger’s blog-quality review of the paper couldn’t find particle counts comparing nanotubes to the controls.  Particle counts may be more important than mass in comparing potency.  The actual particle size on inhalation of nanomaterials will be important.

Eyeballing the charts, all treatments were in the same ball park.  Asbestos at 2 mg was maybe more potent than nanotubes at 2 mg, which were somewhat more potent than ultrafine CB.  But CB was active.

So, nanotubes are maybe less potent than asbestos; not being as dangerous as the worst material in the world is hardly a safe use endorsement.  Carbon black is reliably carcinogenic in the rat and inadequately studied in the mouse;  these findings equate to “possibly carcinogenic” at IARC, and not classifiable at NTP [which demands two species.]  Taking mechanism into account, the Dodger would call nanotubes and CB carcinogenic.

The investigators invoke the “precautionary principle.”  The Dodger opines these data imply carcinogen designation without invoking the PP.  

Toxicology and Applied Pharmacology 207 (2005) 221– 231
Respiratory toxicity of multi-wall carbon nanotubes
Julie Mullera, Franc¸ois Huauxa, Nicolas Moreaub, Pierre Missona, Jean-Franc¸ois Heiliera,
Monique Delosc, Mohammed Arrasa, Antonio Fonsecab, Janos B. Nagyb, Dominique Lisona,T
aIndustrial Toxicology and Occupational Medicine Unit, Universite´ Catholique de Louvain, Clos Chapelle-aux-Champs, 30.54; 1200 Brussels, Belgium
bLaboratory of Nuclear Magnetic Resonance, Faculte´s Universitaires Notre-Dame de la Paix, Namur, Belgium
cLaboratory of Pathology, University Hospital of Mont-Godinne, Yvoir, Belgium
Received 14 September 2004; accepted 5 January 2005
Available online 5 March 2005

Abstract
Carbon nanotubes focus the attention of many scientists because of their huge potential of industrial applications, but there is a paucity of information on the toxicological properties of this material. The aim of this experimental study was to characterize the biological reactivity of purified multi-wall carbon nanotubes in the rat lung and in vitro. Multi-wall carbon nanotubes (CNT) or ground CNT were administered intratracheally (0.5, 2 or 5 mg) to Sprague–Dawley rats and we estimated lung persistence, inflammation and fibrosis biochemically and histologically. CNT and ground CNT were still present in the lung after 60 days (80% and 40% of the lowest dose) and both induced inflammatory and fibrotic reactions. At 2 months, pulmonary lesions induced by CNT were characterized by the formation of collagen-rich granulomas protruding in the bronchial lumen, in association with alveolitis in the surrounding tissues. These lesions were caused by the accumulation of large CNT agglomerates in the airways. Ground CNT were better dispersed in the lung parenchyma and also induced inflammatory and fibrotic responses. Both CNT and ground CNT stimulated the production of TNF-a in the lung of treated animals. In vitro, ground CNT induced the overproduction of TNF-a by macrophages. These results suggest that carbon nanotubes are potentially toxic to humans and that strict industrial hygiene measures should to be taken to limit exposure during their manipulation.

D 2005 Elsevier Inc. All rights reserved. Keywords: Carbon nanotubes; Lung toxicity; Inflammation; Fibrosis  

Comparison of Ergonomic Risk Factors between Men and Women in the Same Workplace

Data reviewed by BrooklynDodger show that women use more disability time than men in blue collar jobs. Other data show that half the time off the job is due to injury and musculoskeletal diagnoses.

Some suggest that not going to work when sick might be related to women living longer, and there is peer reviewed research showing that people who go to work sick die younger.

Hypothetically, increased sickness absense time might arise from women doing more work at home, to lower threshold for taking time off, to taking time off to care for dependents at home.

Another explanation might be differential musculoskeletal risk factors at work. Folk ergonomics preceding the force-frequency-posture paradigm put women in the lower external force jobs, which could hypothetically increase upper extremity risk factors. Reduced body size in relation to workstation design might increase awkwardness of posture. Differential placement in jobs with lower external force, which might involved increased repetition or more time in pinch grip for fine work.

Abstracted below is a study from Sweden - different triggers on taking time off the job - which has limited power. BrooklynDodger forgets the job analysis method, and whether statistical tests were used on this very small cohort. Increased symptoms and increased time off the job were shown for women, although these may not be statistically significant. Increased ergonomic risks to the women were also suggested.


Applied Ergonomics 35 (2004) 521-529
Do work technique and musculoskeletal symptoms differ between men and women performing the same type of work tasks?
Raymond Dahlberg_, Lena Karlqvist, Carina Bildt, Karin Nykvist

National Institute for Working Life, SE-112 79 Stockholm, Sweden
Received 21 November 2002; received in revised form 29 February 2004; accepted 21 June 2004

Â… women worked more frequently and during longer times with their hands above shoulder height than men. Working with hands above shoulder height is considered a risk factor for neck and shoulder disorders according to previous studies. Workplace design factors were probably a reason for differences in working technique between men and women. A higher proportion of women than men reported shoulder symptoms. Women spent more time on household activities than men, which indicates a higher total workload in paid and unpaid work.

The cross-sectional case study took place in a manufacturing company, producing metal sections for the construction industryÂ… All 61 workers in the studied department were invited to take part in the study. Â… 55 (90%) respondedÂ… 32 men and 23 women formed the study group. During the study period, short-time sickness absence (1Â-14 days) was 7.3% of total working time for men and 5.1% for women. Long-time sickness absence (more than 15 days) was 3.5% of total working time for men and 11.7% for women.

Recurring Back Injuries

Despite an abstract which conveys no information [and is not worthy of summary], this publication from Lumbar Motion Monitor central contains important information. Comparing Low Back Pain victims to controls, “the LBP patients experienced higher risk under the same lifting conditions because the patients generated increased spine loading. The increased spine loading in LBP patients compared to asymptomatic controls was due to increased levels of ‘‘guarding’’ or muscle co-activity.”

This provides a physiological explanation, as opposed to psychosocial, for the pattern of recurring back injury among workers.

BrooklynDodger is not sure the investigators have solved the problem of whether the LBP victims showed higher spine loading with similar lifts before their injury, compared to the asymptomatic controls. Other studies show that most injuries arise from “moderate” risk jobs, and that most workers return to the same moderate risk job after return to work.


Applied Ergonomics 36 (2005) 85–95
Workplace design guidelines for asymptomatic vs.
low-back-injured workers
Sue A. Fergusona,_, William S. Marrasa, Deborah Burrb
aBiodynamics Laboratory, Institute for Ergonomics, The Ohio State University, 210 Baker Systems, 1971 Neil Avenue, Columbus, OH 43210, USA
bPublic Health, B110 Star Loving, 320 West 10th Ave, Columbus, OH 43210, USA

One hundred and twenty-three subjects participated in the study. Sixty-two LBP patients and 61 age and gender matched controls. In the patient population there were 32 males and 30 females. The LBP group was diagnosed with muscular LBP and no radiculopathy (diagnosed by their orthopedic surgeon). The median duration of pain symptoms was 5.5 months. Forty-eight percent of the patients had a history of previous LBP. Eighty-eight percent of the patients had returned to work at the time of testing and the median number of lost days from work was 14.

…the LBP patients experienced higher risk under the same lifting conditions because the patients generated increased spine loading (Marras et al., 2001a; Marras et al., 2004a). The increased spine loading in LBP patients compared to asymptomatic controls was due to increased levels of ‘‘guarding’’ or muscle co-activity. The difference influenced the lifting guidelines because in several cases the co-activity in patients created A/P shear levels exceeding 1000N resulting in high-risk classification. Hence, practitioners must be sensitive to the greater loading to which LBP patients are exposed when returning to the workplace. Ergonomists have long argued that it

Fiber Doesn't Reduce Colon Cancer - Another Personal Risk Factor Theory Undermined

Another diet and cancer theory takes a hit. The key findings were : “During follow-up including 1.8 million person-years and 1,596 cases of colorectal cancer, we found little association with fiber intake after controlling for confounding variables.”

Another huge population study comes up empty. How many occupational mortality studies with defined chemical exposures could have been done for this cost.

Cancer Epidemiology Biomarkers & Prevention Vol. 14, 842-849, April 2005© 2005 American Association for Cancer Research
Fiber Intake and Incidence of Colorectal Cancer among 76,947 Women and 47,279 Men
Karin B. Michels1,2,3, Charles S. Fuchs3,5, Edward Giovannucci2,3,4, Graham A. Colditz2,3, David J. Hunter2,3, Meir J. Stampfer2,3,4 and Walter C. Willett2,3,4
1 Obstetrics and Gynecology Epidemiology Center, Department of Obstetrics and Gynecology; 2 Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School; Departments of 3 Epidemiology and 4 Nutrition, Harvard School of Public Health; and 5 Department of Adult Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts


Prospective cohort studies have consistently found no important link between fiber intake and risk of colorectal cancer. The recent large, prospective European Prospective Investigation into Cancer and Nutrition has challenged this paradigm by suggesting significant protection by high fiber intake. We prospectively investigated the association of fiber intake with the incidence of colon and rectal cancers in two large cohorts: the Nurses' Health Study (76,947 women) and the Health Professionals Follow-up Study (47,279 men). Diet was assessed repeatedly in 1984, 1986, 1990, and 1994 among women and in 1986, 1990, and 1994 among men. The incidence of cancer of the colon and rectum was ascertained up to the year 2000. Relative risk estimates were calculated using a Cox proportional hazards model simultaneously controlling for potential confounding variables. During follow-up including 1.8 million person-years and 1,596 cases of colorectal cancer, we found little association with fiber intake after controlling for confounding variables. The hazard ratio for a 5-g/d increase in fiber intake was 0.91 (95% confidence interval, 0.87-0.95) after adjusting for covariates used in the European Prospective Investigation into Cancer and Nutrition study and 0.99 (95% confidence interval, 0.95-1.04) after adjusting for additional confounding variables. Our data from two large prospective cohorts with long follow-up and repeated assessment of fiber intake and of a large number of potential confounding variables do not indicate an important association between fiber intake and colorectal cancer but reveal considerable confounding by other dietary and lifestyle factors.

AC”S””H” and the Information Quality Act

For years public health advocates have struggled with the new EPA carcinogen guidelines in draft form. Basically, the guidelines flung open the door to Houdini Risk Assessments based on “mechanism.” The guidelines also introduce a new set of terms and definitions for levels of evidence divergent from NTP [statutory], IARC [customary], OSHA [regulatory], ACGIH [obscure].

Now comes the premier “money tox” organization, the American Council on “Science” and “Health.” The AC”S””H” has petitioned in terms of the Information Quality Act to overturn these guidelines.

BrooklynDodger thinks the response needs two prongs. First, figuring out where these IQA appeals go, and who decides them. Second, approaching those associated with the AC”S””H” who pretend to scientific qualifications, such as the Board of Directors members who aren’t lobbyists, and the Scientific Advisors. The issue with these folks is whether the petition itself was peer reviewed within the terms of the IQA.

If you recognize any of the names below, you might email them with the question.

ACSH Petitions EPA to Stop Declaring Chemicals "Carcinogens" Based on Rodent Tests Alone


PRESS RELEASE Publication Date: August 23, 2005
New York, NY -- August 23, 2005. The American Council on Science and Health (ACSH) today petitioned the Environmental Protection Agency (EPA) to eliminate "junk science" from the process by which it determines whether a substance is likely to cause cancer in humans.
The petition, filed on behalf of ACSH by the Washington Legal Foundation (WLF), a public interest law firm, argues that current EPA guidelines violate the Information Quality Act (IQA) -- the law that requires the federal government to ensure the "equality, objectivity, utility, and integrity" of information it dispenses to the public.

Board of Directors:

http://www.acsh.org/about/pageID.7/default.asp

Scientific Advisors:

http://www.acsh.org/about/pageID.89/default.asp

Stress and MI - Lancet

Another paper linking psychosocial risk factors, especially stress at work, to MI’s. BrooklynDodger actually hesitated because the cross cultural issues might obscure an effect, but neverthe less an effect was found.

The Lancet Volume 364, Issue 9438 , 11 September 2004-17 September 2004, Pages 953-962

Association of psychosocial risk factors with risk of acute myocardial infarction in 11 119 cases and 13 648 controls from 52 countries (the INTERHEART study): case-control study

ProfAnnika Rosengren MDb, Steven Hawken MSca, Stephanie Ôunpuu PhDa, ProfKaren Sliwa MDc, Mohammad Zubaid MDd, Wael A Almahmeed MDf, ProfKathleen Ngu Blackett MDe, ProfChitr Sitthi-amorn MDg, Hiroshi Sato MDh, ProfSalim Yusuf FRCP, a, and for the INTERHEART investigators aMcMaster University, Hamilton Health Sciences, Hamilton, ON, CanadabSahlgrenska University Hospital/Ostra, Göteborg, SwedencBaragwanath Hospital, Johannesburg, South AfricadKuwait University, Kuwait City, KuwaiteCHU, Yaoundé, CameroonfAl-Jazeira and Central Hospitals, Abu Dhabi, United Arab EmiratesgDepartment of Medicine, Chulalongkorn University, Bangkok, ThailandhOsaka University Graduate School of Medicine, Suita, Japan

.... We used a case-control design with 11119 patients with a first myocardial infarction and 13648 controls from 262 centres in Asia, Europe, the Middle East, Africa, Australia, and North and South America. …Psychosocial stress was assessed by four simple questions about stress at work and at home, financial stress, and major life events in the past year. Additional questions assessed locus of control and presence of depression.
People with myocardial infarction (cases) reported higher prevalence of all four stress factors (p<0·0001). …[Elevated risks were found for] several periods of work stress……permanent work stress during the previous year .. several periods of work stress … permanent stress at work…Cases had several periods of stress at home,… permanent stress at home … General stress (work, home, or both) … Severe financial stress w… Stressful life events in the past year …[and] depression (24·0% [2673] vs 17·6% [2404]; odds ratio 1·55 [1·42–1·69]). These differences were consistent across regions, in different ethnic groups, and in men and women.
Interpretation
Presence of psychosocial stressors is associated with increased risk of acute myocardial infarction, suggesting that approaches aimed at modifying these factors should be developed.

Gun Ownership in US Households

From time to time, mortality studies among industrial workers show increased mortality from external causes, homicides and suicides. A large risk factor for being killed by a gun is having one in the house, Therefore, regional and class differences in prevalence of guns in the house is important to interpreting these data.

These investigators conducted a review, and concluded that published studies indicate that firearms are present in about one third of U.S. households. Handguns in particular are present in more than half of U.S. households with firearms, or about 19% of all U.S. households. The prevalence of firearms and handguns in households with young people was similar to the prevalence overall. The prevalence of firearm ownership was highest in the South, followed by states in the Midwest; firearm ownership in those two regions ranged from 40% to 55%.

They opined “firearms are common in U.S. households, even in the homes of medical professionals and those with children.”

Despite reference to storage practices in the title, there’s nothing much in the abstract. Safety advocates stress keeping the guns in one safe, the ammo in another. BrooklynDodger recalls the NRA advocating keeping ammo out of guns except when the guns are in use; if the use of the gun is self-defense, then it can be loaded, which is all the time.

PS: Why are review articles title “systematic review” or “critical review?” Do journals publish unsystematic and uncritical reviews? Reviewers of review articles ought to look into this. Or editors of journals.


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

Am J Prev Med. 2004 Aug;27(2):173-82.
Firearm ownership and storage practices, U.S. households, 1992-2002. A systematic review.Johnson RM, Coyne-Beasley T, Runyan CW.

Injury Prevention Research Center, School of Public Health, Department of Health Behavior and Health Education, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.

BACKGROUND: Because the presence and improper storage of household firearms are risk factors for injury, it is important to understand the prevalence of ownership and storage practices within households to help guide intervention development. This systematic review of published articles (1992 to 2002) provides prevalence estimates of firearm ownership and storage practices in U.S. households. METHODS: A search of bibliographic databases (MedLine, CINAHL, PsycInfo, Sociological Abstracts) was completed in January 2003. RESULTS: Although all were cross-sectional, the 42 articles included in this review varied in type; there were seven national and five state prevalence studies, as well as studies using clinic-based convenience samples (n =14) and samples of professionals (n =10). Published studies indicate that firearms are present in about one third of U.S. households. Handguns in particular are present in more than half of U.S. households with firearms, or about 19% of all U.S. households. The prevalence of firearms and handguns in households with young people was similar to the prevalence overall. Firearm ownership was highest in the South. “The prevalence of firearm ownership was highest in the South, followed by states in the Midwest; firearm ownership in those two regions ranged from 40% to 55%

CONCLUSIONS: Although the methodologic rigor of published articles varies substantially, the literature clearly establishes that firearms are common in U.S. households, even in the homes of medical professionals and those with children.

More costs of the first Gulf War

More costs of the first gulf war.

The study by the VA contacted 11,441 Gulf War Respondents out of 15,000 targeted.

Male Gulf war respondents demonstrated 11.2% PTSD compared to 15.8% among females. Among 189 females reporting no sexual harassment or assault, the rate of PTSD was about 11%. Among the 116 females reporting sexual harassment, assault, or both, the PTSD rate was about 26%. Maybe it’s not a surprise that sexual predation would increase PTSD. That 116/336 or 34% of female veterans reported incidents, is a bit of a surprise, something which should have been in the abstract.

Annals of Epidemiology Volume 15, Issue 3 , March 2005, Pages 191-195
The Role of Sexual Assault on the Risk of PTSD among Gulf War Veterans
Han Kang DrPH, , Nancy Dalager MS, Clare Mahan PhD and Erick Ishii PhD From the Veterans Health Administration, Department of Veterans Affairs, Washington, DC Received 11 December 2003; accepted 25 May 2004. Available online 6 August 2004.
A nested case–control analysis was conducted using the data collected in a population-based health survey of 30,000 Gulf War era veterans. A total of 1381 Gulf War veterans with current PTSD were compared with 10,060 Gulf veteran controls without PTSD for self-reported in-theater experiences of sexual harassment/assault and combat exposure.
…
The adjusted odds ratio (aOR) for PTSD associated with a report of sexual assault was 5.41 (95% confidence interval [CI], 3.19–9.17) in female veterans and 6.21 (95% CI, 2.26–17.04) in male veterans. The OR for PTSD associated with “high” combat exposure was also statistically significant (OR, 4.03 [95% CI, 1.97–8.23] for females; OR, 4.45 [95% CI, 3.54–5.60] for males).
Conclusion
Notwithstanding a possibility of recall bias of combat and sexual trauma, for both men and women, sexual trauma as well as combat exposure appear to be strong risk factors for PTSD.

Emergency Room vs. BLS Occupational Injury Rates

This not so old publications looks back at the relationship between BLS data and reality. Investigator initiated research likely provides better data, even heavily modeled or extrapolated, than the BLS census-sampling approach based on employer reported data.

BrooklynDodger speculates that injuries treated in emergency departments are a more severe minority fraction of all injuries, and especially occupational injuries. Less severe and less emergent injuries would be treated in facility medical by nursing staff, diverted to industrial clinics or non-hospital urgent care facilities, or, for musculoskeletal conditions, physicians’ offices.

The most reliable result is that strain-sprain injuries dominated even this fraction of injuries.

BrooklynDodger factions with those who believe employer reports to BLS substantially undercount injuries. Somehow, the ED extrapolation is 3.3 million injuries in a year when BLS estimated 6.2. BrooklynDodger would have expected a higher BLS/ED ratio. The ED/BLS rates are a bit less divergent from expection: 2.8 for ED’s v. 7.2 for BLS, a higher ratio of BLS.
Surveillance for Nonfatal Occupational Injuries Treated in Hospital Emergency Departments -- United States, 1996
An estimated 3.3 million persons aged greater than or equal to 16 years were treated for occupational injuries in EDs in the United States during 1996, yielding an average crude annual rate of 2.8 injuries per 100 FTEs (95% CI=2.2-3.3). Physician-diagnosed sprains and strains accounted for 27% of the injuries, followed by lacerations (22%) and contusions/abrasions/hematomas (20%). Lacerations to the hands and fingers accounted for 15% of all injuries, and sprains and strains to the back, groin, and trunk accounted for an additional 12% of all cases treated in hospital EDs.

In 1996, data from the BLS annual survey show that 6.2 million injuries and illnesses occurred in the private sector, for an incidence rate of 7.4.

The World of BLS Injury Rates: Where Every Employer is Better than the Average

The World of BLS Injury Rates:  Where Every Employer is Better than the Average

The BLS injury rate measures the risk of injury for an individual worker.  It compares that risk between industry sectors and facility sizes.  Data quality problems with unaudited employer reports aside, there’s some value to that number.  

The BLS number distinctly not appropriate for it’s most common use, which is inferring safety performance of a facility by comparing the facility’s incidence rate to the national “average” or some multiple of the national average.  Facilities get awards, recognition, exclusion from scheduled OSHA inspections for this.  Legislation is frequently introduced to reduce OSHA penalties.

The “average” or “arithmetic mean” is appropriate for data which follow a normal distribution.  Half the sample will have values above, and half below the mean, which will approximate the median or midpoint of the distribution.  Facility injury rates are distinctly skewed, so the arithmetic mean is distinctly inappropriate.

The distribution of incidence rates across facilities by industry sector and size is published annually by the Bureau of Labor Statistics.  The most recent data are for 2003, posted at http://stats.bls.gov/iif/oshwc/osh/os/ostb1359.txt.  

Employers who manage more than three-fourths of American worksites report no injuries at all.  Because these data are displayed only in quartiles, we can’t estimate whether the no-injury cut point is 85th percentile, 90th percentile, 95th percentile or higher.  The national “average” [all private employement] is 5.0 workers injured and recorded per 100 employees.  Obviously the average (mean) is far above the median.  Since the median is also zero, the ratio of the average to the median is indeterminate.   For workplaces with less than 50 employees, the median is zero, with the no-injury cut point somewhere between 50th percentile and 75th percentile.  The next larger size ranges are 50-249, 250-999, and greater than 1000.  For each of these, the average is 128%, 145% and 157% of the median.  

For the manufacturing sector as a whole, where the national average is 8.1 workers injured and recorded per 100 employees, the median injury rate is zero, the 75th percentile facility carries an incidence rate well below the average.   The no-injury cut point is somewhere between the 50th and 75th percentile, and no ratio of average to median can be calculated for workplaces with less than 50 employees.  For the next larger size ranges, the average is 124%, 125% and 171% of the median.

We note that distributions for recorded Lost Workday case rates and recorded LWD cases with days away from work are even more skewed that the rates for total recordable cases.

The take home lesson is that being better than the national “average” is a pretty poor benchmark for a criterion for facility.

Information Quality Act Appeal Tries to Put Naphthalene in Moth Balls

BrooklynDodger was wandering the NIEHS website and encountered yet a new front in public health policy. People - industry - can appeal virtually any publication on health hazards. This post has to do with listing of naphthalene as "reasonably anticipated to be a human carcinogen" in the NTP Report on Carcinogens.

Naphthalene -- Information Quality Act Request for Reconsideration

IARC monographs and Report on Carcinogens listings serve two functions. The public health function is warning the public of chemicals which pose a carcinogenic hazard.

Another function is determining whether data on a chemical meet the criteria for declaring a chemical as known to be carcinogenic in humans, or reasonably anticipated [NTP] or probably or possibly [IARC] carcinogenic. An ongoing scientific project compares the laboratory evidence for known human carcinogens to the human evidence. Agents which behave in the laboratory similarly to those agents known to be carcinogenic in humans ought to be assumed to pose the same risk in humans, with or without a body count. Scientific evaluation of data against the criteria for assessment serves this purpose.

Attacks on the public health front, fomented by economic interests, threaten to undermine the scientific project as well.

So here comes naphthalene. Since BrooklynDodger was a pup, multi-ringed (5 ringed) polynuclear aromatic compounds were considered the bad boys; lower ringed compounds, presumably more plentiful in smoke and soot, were discounted.

The single ring, benzene, sat in the corner as the bad boy of the aromatic sequence. Naphthalene, anthracene, pyrene [not sure if the Dodger has this progression right] were neutral, and then benzopyrene was the biggest bad boy.

Now, there is some evidence that naphthalene vapor causes lung tumors in female but not male mice, and clear evidence that napthalene causes nasal tumors in rats of both genders. The mouse tumors face the "not relevant to humans" eraser by the mouse clara cell hypothesis, this years HRA [Houdini Risk Assessment] model. By NTP criteria, two species are needed for reasonably, so if the mice are erased, so is "reasonably." By IARC criteria, two studies are needed for possibly, the male and female rats are considered one study, so if the mice go, so does "possibly."

Prior to MEGO [my eyes glazed over], it appeared the industry appeal, and appeal of denial, are entirely based on procedure and not substance.

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TR-410
Toxicology and Carcinogenesis Studies of Naphthalene (CAS No. 91-20-3) in B6C3F1 Mice (Inhalation Studies)

Under the conditions of these 2-year inhalation studies, there was no evidence of carcinogenic activity of naphthalene in male B6C3F1 mice exposed to 10 or 30 ppm. There was some evidence of carcinogenic activity of naphthalene in female B6C3F1 mice, based on increased incidences of pulmonary alveolar/ bronchiolar adenomas.
In both male and female mice, naphthalene caused increased incidences and severity of chronic inflammation, metaplasia of the olfactory epithelium, and hyperplasia of the respiratory epithelium in the nose and chronic inflammation in the lungs.

TOXICOLOGY AND CARCINOGENESIS
STUDIES OF NAPHTHALENE
(CAS NO. 91-20-3)
IN F344/N RATS
(INHALATION STUDIES)
NTP TR 500


CONCLUSIONS
Under the conditions of this 2-year inhalation study,
there was clear evidence of carcinogenic activity* of
naphthalene in male and female F344/N rats based on
increased incidences of respiratory epithelial adenoma
and olfactory epithelial neuroblastoma of the nose.
In male and female rats, exposure to naphthalene
caused significant increases in the incidences of nonneoplastic
lesions of the nose.

Guns in the Home - Self Offense

CDC investigators concluded that persons with guns in the home were at about twice the greater risk of dying from a homicide in the home. than those without guns in the home. The risk of dying of a firearm homicide at home was 16 fold for persons 35 and older with a firearm in the home compared to those without. The risk of dying from a suicide in the home was 10 times greater for males in homes with guns than for males without guns in the home. Regardless of storage practice, type of gun, or number of firearms in the home, having a gun in the home was associated with an increased risk of firearm homicide and firearm suicide in the home. Homicide victims were mostly male, less than 35 years of age, and of racial or ethnic minority status. Suicide victims were predominately male, older, and non-Hispanic White.



Related Articles,(image placeholder)Links

Guns in the home and risk of a violent death in the home: findings from a national study.Dahlberg LL, Ikeda RM, Kresnow MJ.Division of Violence Prevention, National Center for Injury Prevention and Control, Centers for Disease Control and Prevention, Atlanta, GA 30341, USA. ldahlberg@cdc.govData from a US mortality follow-back survey were analyzed to determine whether having a firearm in the home increases the risk of a violent death in the home and whether risk varies by storage practice, type of gun, or number of guns in the home. Those persons with guns in the home were at greater risk than those without guns in the home of dying from a homicide in the home (adjusted odds ratio = 1.9, 95% confidence interval: 1.1, 3.4). They were also at greater risk of dying from a firearm homicide, but risk varied by age and whether the person was living with others at the time of death. The risk of dying from a suicide in the home was greater for males in homes with guns than for males without guns in the home (adjusted odds ratio = 10.4, 95% confidence interval: 5.8, 18.9). Persons with guns in the home were also more likely to have died from suicide committed with a firearm than from one committed by using a different method (adjusted odds ratio = 31.1, 95% confidence interval: 19.5, 49.6). Results show that regardless of storage practice, type of gun, or number of firearms in the home, having a gun in the home was associated with an increased risk of firearm homicide and firearm suicide in the home.

Population Injury Data

BrooklynDodger returns to off-the-job injuries. Occupational health staff are being pressured to generate off-the-job injury programs. To avoid pure blame the victim approaches, and to consider the hierarchy of controls, it would be valuable to know something about these off-the-job injuries. The Dodger notes that many “off-the-job” injuries are actually on-the-job injuries carried home and treated away from work. These on-job caused injuries may be off-job treated to hide them from punitive employer programs, or just because it’s more convenient and with more patient control to go outside.

The Consumer Product Safety Commission (CPSC) National Electronic Injury Surveillance System (NEISS) collects data on all types and external causes of nonfatal injuries and poisonings treated in U.S. hospital emergency departments (EDs). Approximately 31,000,000 persons were treated for nonfatal injuries in EDs in 2000. Most of the injuries were unintentional. Only... an estimated 1,973,000 (6.4%) were violence-related.

[ICD-9-CM external cause-of-injury codes were not assigned. Safety folks should review these causes for utility in the occupational setting.]

During 2000, an estimated rate of 11,188 per 100,000 population were treated, over 10%. The nonfatal injury rate was approximately 40% higher for males than for females. Falls were the leading cause of unintentional nonfatal injuries, 24.4%. About 17% were transport related. Overexertion caused 10.5% of cases. These cause codes are somewhat informative about prevention of injury. Other causes, such as struck by, at 17.4%, were not informative.
CPSC maintains an open website somewhere for generating reports at

http://www.cpsc.gov/library/neiss.html.

These queries could generate data on working age people, to inform off-the-job safety programs delivered on job. BrooklynDodger has not been very successful using this site.


National Estimates of Nonfatal Injuries Treated in Hospital Emergency Departments --- United States, 2000
Reported by: Office of Statistics and Programming, National Center for Injury Prevention and Control, CDC.

Injury Prevention and Guns

BrooklynDodger hears the argument for gun possession being self protection.

CDC investigators concluded that persons with guns in the home were at about twice the greater risk of dying from a homicide in the home than those without guns in the home. Suicide risk was much greater. The risk of dying of a firearm homicide at home was 16 fold for persons 35 and older with a firearm in the home compared to those without. The risk of dying from a suicide in the home was 10 times greater for males in homes with guns than for males without guns in the home. Regardless of storage practice, type of gun, or number of firearms in the home, having a gun in the home was associated with an increased risk of firearm homicide and firearm suicide in the home. Homicide victims were mostly male, less than 35 years of age, and of racial or ethnic minority status. Suicide victims were predominately male, older, and non-Hispanic White.


Am J Epidemiol. 2004 Nov 15;160(10):929-36.

Guns in the home and risk of a violent death in the home: findings from a national study.

Dahlberg LL, Ikeda RM, Kresnow MJ.Division of Violence Prevention, National Center for Injury Prevention and Control, Centers for Disease Control and Prevention, Atlanta, GA 30341, USA. ldahlberg@cdc.gov

Data from a US mortality follow-back survey were analyzed to determine whether having a firearm in the home increases the risk of a violent death in the home and whether risk varies by storage practice, type of gun, or number of guns in the home. Those persons with guns in the home were at greater risk than those without guns in the home of dying from a homicide in the home (adjusted odds ratio = 1.9, 95% confidence interval: 1.1, 3.4). They were also at greater risk of dying from a firearm homicide, but risk varied by age and whether the person was living with others at the time of death. The risk of dying from a suicide in the home was greater for males in homes with guns than for males without guns in the home (adjusted odds ratio = 10.4, 95% confidence interval: 5.8, 18.9). Persons with guns in the home were also more likely to have died from suicide committed with a firearm than from one committed by using a different method (adjusted odds ratio = 31.1, 95% confidence interval: 19.5, 49.6). Results show that regardless of storage practice, type of gun, or number of firearms in the home, having a gun in the home was associated with an increased risk of firearm homicide and firearm suicide in the home.

Money Tox - Cambridge Envronmental Against Diesel

BrooklynDodger found this abstract when looking up precedents for Cambridge Environmental. But the comparison of cigarette smoke and diesel particulate matter instructs.

The effect level for lung cancer for diesel in a rat bioassay is around 5 mg/m3. For tobacco smoke it's upwards of 100 mg/m3. Cigarette smoke is virtually impotent compared to occupational agents and air pollution in general.

Cigarette carcinogenesis has been framed as a mutagenicity effect. Here, likely hired by the diesel engine manufacturers, Cambridge demonstrates that mutagenicity is about equal. Nevertheless, diesel is way more potent in the bioassay, and, if you believe the epidemiology of truck drivers and train drivers, way more potent in people.

It follows that mutagenic potential is not the driving force, and particles are.


>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
Inhal Toxicol. 1999 Mar;11(3):215-28.

Comparative mutagenic dose of ambient diesel engine exhaust.

Valberg PA, Watson AY.
Cambridge Environmental, Inc.,
58 Charles Street, Cambridge, MA 02141, USA.

pvalberg@hsph.harvard.edu

Diesel engine exhaust contains carbon-based particles that can be inhaled and deposited on lung surfaces. Concern about the carcinogenic potential of diesel engine exhaust derives in part from the mutagenic activity of organics that can be extracted from exhaust particles. However, the lung cancer risk is controversial, and diesel exhaust is a candidate for further evaluation. A comparative potency approach can be used to rank the mutagenic risk of diesel exhaust with other combustion products. We compared the specific mutagenic activities of cigarette smoke condensate (CSC) and diesel exhaust particle extract (DEPE) and estimated "mutagenic dose" to the lungs. Although the specific mutagenic activities of CSC and DEPE are similar in magnitude, it is the dose reaching the lungs that is more relevant for comparing mutagenic potential. We calculated that, depending on the source of CSC and DEPE, a person would have to inhale approximately 63 to 181 mg of particulate from diesel engine exhaust to match the mutagenic dose of 1 cigarette. We also calculated that a person would have to breathe diesel exhaust (1.5 microg/m(3), estimated total personal exposure) for 6 to 16 yr to equal the mutagenic dose of 1 cigarette. Although instructive, comparative potency results should be used cautiously due to the need for simplifying assumptions. For example, the type of mutagenic assay and the source of cigarettes and diesel engine exhaust could affect dose estimates to some degree; however, the extent to which diesel particle mutagens are bioavailable would have an even greater effect on estimates of relative risk. For both cigarette smoke and diesel exhaust particles, we assumed that the organic mutagens are 100% bioavailable. In summary, our analysis showed a larger mutagenic dose-to-target-tissues in the smoke of one cigarette as compared to a year of exposure to diesel exhaust particulate at ambient levels.

Is Depleted Uranium the New Agent Orange?

Depleted uranium is getting a lot of play as the new Agent Orange. BrooklynDodger is still agnostic on this question.

That's why BrooklynDodger posted the abstract below, although the Dodger confesses to not reading the full text. BrooklynDodger is puzzled how a 144 ug/kg dose in the rat could generate a 2.6 ug/g or 2600 ug/kg concentration in the kidney as quoted in the abstract. Perhaps a misprint, now traversing the globe as a virus in the abstract spread by medline? Or a notable concentration effect.

BrooklynDodger understands the notable use of DU is a kinetic energy round: jacketed by steel, an artillery sheel cored with DU penetrates armor, releasing hot uranium which burns inside the other guy's tank. DU rounds hitting targets - estimated at 10% of what's shot off - would generate uranium oxide fume in some quantity. DU rounds which missed might be lying on the ground, and perhaps further dispersed by explosives in the warhead, even as uranium oxide. BrooklynDodger also understands that DU is used in the armor itself, sandwiched between steel to resist and react to penetration by the other guy's shells hitting our guy's armored vehicles.

Apparently there is a lot of DU around for non warlike uses. There's also a lot of undepleted uranium around in dirt, not concentrated enough to be recovered, but enough to generate some background radioactivity.

Absorbed DU is the issue; alpha particles don't penetrate the skin much. Absorbed DU ought to be easy to find through urine testing. Here's the best that BrooklynDodger could do with minimal effort:

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

BIOLOGIC MONITORING FOR URINARY URANIUM IN GULF WAR I VETERANS.
Health Physics. 87(1):51-56, July 2004.
McDiarmid, Melissa A. *; Squibb, Katherine +; Engelhardt, Susan M. ++

...Two hundred and twenty-seven veterans submitted samples for analysis from January 2000 through December 2002, which included a 24-h urine sample for determination of total urinary uranium concentration and completed questionnaires describing their wartime exposure experiences. Thirty questionnaire items characterizing DU exposure opportunities were collapsed into 19 exposure categories. Urine uranium (U) results were stratified into low and high uranium groups with 0.05 [mu]g U g-1 creatinine as the cut point. Exposure scenarios in the high and low uranium groups were similar in frequency and type with only the presence of retained shrapnel being predictive of a high urine uranium value, as found in the first phase of this surveillance of 169 veterans performed prior to 2000. Twenty-two veterans exhibited U levels in the high range. Isotopic analysis, available for 21 of these 22, revealed that all but three of these samples contained natural and not depleted uranium. These three participants had retained DU shrapnel as a result of their past injuries. Thus, even with an enlarged cohort, elevated urine uranium values in the absence of retained DU fragments are unlikely. The utility of isotopic analysis to more fully characterize uranium biomonitoring results is also demonstrated. Health Phys.

BrooklynDodger hasn't read the full text. Exposure histories were misleading in relation to agent Orange.

>>>>>>>>>>>>>
Toxicology Volume 212, Issues 2-3 , 1 September 2005, Pages 219-226

The brain is a target organ after acute exposure to depleted uranium
P. Lestaevela, , , P. Houperta, C. Bussya, B. Dhieuxa, P. Gourmelonb and F. Paqueta a

Institut de Radioprotection et de Sûreté Nucléaire, Département de Radio-Protection de l’Homme, Laboratoire de Radio-Toxicologie Expérimentale, BP 166, 26702 Pierrelatte, FrancebInstitut de Radioprotection et de Sûreté Nucléaire, Département de Radio-Protection de l’Homme, BP 6, 92265 Fontenay aux Roses, France

The health effects of depleted uranium (DU) are mainly caused by its chemical toxicity. Although the kidneys are the main target organs for uranium toxicity, uranium can also reach the brain. In this paper, the central effects of acute exposure to DU were studied in relation to health parameters and the sleep–wake cycle of adult rats. Animals were injected intraperitoneally with 144 ± 10 μg DU kg−1 as nitrate. Three days after injection, the amounts of uranium in the kidneys represented 2.6 μg of DU g−1 of tissue, considered as a sub-nephrotoxic dosage. The central effect of uranium could be seen through a decrease in food intake as early as the first day after exposure and shorter paradoxical sleep 3 days after acute DU exposure (−18% of controls). With a lower dosage of DU (70 ± 8 μg DU kg−1), no significant effect was observed on the sleep–wake cycle. The present study intends to illustrate the fact that the brain is a target organ, as are the kidneys, after acute exposure to a moderate dosage of DU. The mechanisms by which uranium causes these early neurophysiological perturbations shall be discussed.

Family Values in Mesothelioma

The Specter-Lahey Bill, just reported from the Senate Judiciary Committee, has provisions for familial [take home exposure] asbestos cases.

BrooklynDodger was unable to access the full text of this paper, which has maybe not the best abstract. These are italian data. Of 610 cases, 40 had familial cases. Of the 40, 25 had no blood relationship. It's reported these were all exposed occupationally, and no take home cases are being reported. Latency periods (time intervals between first exposure to asbestos and diagnosis) ranged between 25 and 70 yr (mean 52.0, median 54.0).

BrooklynDodger is all mixed up here. The 40 familial cases, 20 pairs might have had some take home asbestos effect.

There were 530 victims with no familial case. The 530 likely had high asbestos exposure at work and therefore an opportunity to take home. The upper 95% CI on 0/530 is 0.0056. Does this mean we are 95% confident that the mesothelioma risk from take home asbestos for workers with high enough exposure to get mesothelioma is less than .6%?

The median latency may be of value in estimating future meso risk. 55 plus 1945 = 2000; the midpoint of the cases for WW II ship building would have been somewhere before 2000.

>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
Ind Health. 2004 Apr;42(2):235-9.
Familial mesothelioma of the pleura--a report of 40 cases.

Bianchi C, Brollo A, Ramani L, Bianchi T, Giarelli L.

Center for the Study of Environmental Cancer, Laboratory of Pathological Anatomy, Hospital of Monfalcone, 34074 Monfalcone, Italy.

A survey of 610 pleural mesotheliomas disclosed 40 familial cases. ... Occupational data were collected from the patients or from their relatives by personal interviews. Routine lung sections were examined for asbestos bodies in 32 cases. In 15 cases asbestos bodies were isolated after chemical digestion of lung tissue. Familial mesotheliomas included 31 men and 9 women ... In 15 families there were blood relations between (or among) the members involved. [ And 25 not, so the majority had no genetic component.] All the patients had been exposed to asbestos, mostly in the shipyards. Asbestos bodies were found on routine lung sections in 27 cases. Asbestos bodies after isolation ranged from 70 bodies to about 900,000/g dried lung tissue. Latency periods (time intervals between first exposure to asbestos and diagnosis) ranged between 25 and 70 yr (mean 52.0, median 54.0). The occurrence of mesothelioma among subjects with blood relations suggests that genetic factors might play a role in determining the susceptibility to asbestos-related cancer. Familial cases among persons without blood relations raise the question if environmental factors that members of a family share, may act as co-factors in asbestos-related mesothelioma.

Modeling Lower Dose Cancer Risk After Effects are Found at Directly Observable Levels

BrooklynDodger argues that the shape of the exposure response relationship for carcinogens in the region where that relationship can't be directly observed decides the high dose-low dose extrapolation which is critical to public health interventions. Does the curve go through zero dose [therefore every reduction has a benefit], or is there a practical threshold [a region where there is no dose response relationship]?

It's generally accepted that genotoxic - somatic mutagenic - carcinogens don't show a threshold. Houdini risk assessments can still make the low dose risk go away through other means, but extra mathematical means.

The two natural experiments, environmental tobacco smoke and lung cancer, and take home asbestos and mesothelioma, demonstrate no threshold, or at least risk persisting to low fractions of the previously known hazard level. Asbestos is not conventionally genotoxic [ames test positive.] Tobacco smoke is ames test positive, but is also a promoter.

David Gaylor is a Jedi among modelers. While at NCTR, he seemed often intuned to the bright side of the public health force. A few key quotes ripped from the abstract:

"However, a threshold dose is questionable if a nongenotoxic carcinogen acts via a cell receptor. Also, a nongenotoxic carcinogen that increases the cell proliferation rate, via the cell division rate and/or cell removal rate by apoptosis, by augmenting an existing endogenous mechanism is not likely to have a threshold dose."

"small changes in the cell proliferation rate, that may be obscured by the background noise in rates, can produce large changes in the lifetime tumor incidence as calculated from the Moolgavkar-Venzon-Knudson model. That is, dose response curves for cell proliferation and tumor incidence do not necessarily mimic each other. This makes the use of no observed effect levels (NOELs) for cell proliferation rates often inadmissible for establishing acceptable daily intakes (ADIs) of nongenotoxic carcinogens."

Application of EPA-IRIS style safety factors to most carcinogenicity bioassay data, and all human epidemiology data, projects to drastrically reduced PEL's compared to what prevail now.

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Risk Anal. 1996 Apr;16(2):221-5.

Risk assessment of nongenotoxic carcinogens based upon cell proliferation/death rates in rodents.

Gaylor DW, Zheng Q.

Division of Biometry and Risk Assessment, National Center for Toxicological Research, U.S. Food and Drug Administration, Jefferson, Arkansas 72079, USA.

Increased cell proliferation increases the opportunity for transformations of normal cells to malignant cells via intermediate cells. Nongenotoxic cytotoxic carcinogens that increase cell proliferation rates to replace necrotic cells are likely to have a threshold dose for cytotoxicity below which necrosis and hence, carcinogenesis do not occur. Thus, low dose cancer risk estimates based upon nonthreshold, linear extrapolation are inappropriate for this situation. However, a threshold dose is questionable if a nongenotoxic carcinogen acts via a cell receptor. Also, a nongenotoxic carcinogen that increases the cell proliferation rate, via the cell division rate and/or cell removal rate by apoptosis, by augmenting an existing endogenous mechanism is not likely to have a threshold dose. Whether or not a threshold dose exists for nongenotoxic carcinogens, it is of interest to study the relationship between lifetime tumor incidence and the cell proliferation rate. The Moolgavkar-Venzon-Knudson biologically based stochastic two-stage clonal expansion model is used to describe a carcinogenic process. Because the variability in cell proliferation rates among animals often makes it impossible to detect changes of less than 20% in the rate, it is shown that small changes in the cell proliferation rate, that may be obscured by the background noise in rates, can produce large changes in the lifetime tumor incidence as calculated from the Moolgavkar-Venzon-Knudson model. That is, dose response curves for cell proliferation and tumor incidence do not necessarily mimic each other. This makes the use of no observed effect levels (NOELs) for cell proliferation rates often inadmissible for establishing acceptable daily intakes (ADIs) of nongenotoxic carcinogens. In those cases where low dose linearity is not likely, a potential alternative to a NOEL is a benchmark dose corresponding to a small increase in the cell proliferation rate, e.g., 1%, to which appropriate safety (uncertainty) factors can be applied to arrive at an ADI.

EPA Fine Particles - Buckle on your Chin Strap

News for Release: Friday, July 1, 2005
U.S. Environmental Protection Agency (EPA)
Final EPA Staff Paper Recommends Stronger Particle Pollution Standards

A big shoe dropped early in July, and few heard it fall. EPA released a staff draft document on particle pollution. OSHAniks will not recognize this in procedure, it's like publishing as a pre-preamble, for comment, the recommendation by OSHA staff to the Assistant Secretary. Apparently EPA is under court order to issue a proposal for particulate limits by December 2005 and a final rule by September 2006.

This will be a reengagement of the huge fight of a few years ago, when EPA attempted a small particle standard that was essentially equivalent to the then coarse particle standard.

The staff document, 512 pdf pages, frustrates a reader looking for the beef. As best BrooklynDodger could find, the meat is this.

EPA staff recommend mildly improve limits based on "the evidence of mortality and morbidity effects in areas where the current standards were met." Permitted averages are not much changed, but daily excursions above those averages are likely the targets.

Proposed changes are not very protective, they are actually effect levels for increased mortality.

Stay tuned for the next battle.


Contact: John Millett 202-564-4355 / millett.john@epa.gov
(Washington, D.C.-July 1, 2005)

A key document in EPA's review of
national air quality standards for particle pollution recommends the
administrator consider strengthening and refining current standards to
better protect public health and visibility...The Clean Air Act requires EPA to periodically review air quality standards to ensure they provide adequate health and environmental
protection and to update those standards if necessary. In December
2004, EPA and states began implementing the first fine particle standard
when the agency designated areas of the country that require additional
local, state and federal steps to reduce PM 2.5.
... the staff paper concludes
that the latest scientific, health and technical information about
particle pollution supports strengthening EPA's current health-based
standards for fine particles. ...

The staff paper recommends that EPA continue to regulate but revise the
current PM10 standards with a new health-based standard for particles
known as "thoracic coarse" particles -- particles between 2.5 and 10
micrometers in diameter that can be deeply inhaled. Staff recommends
that such a standard apply to more toxic urban coarse particles.
...
The agency is required by a consent decree to issue a
proposal regarding the particle pollution standards by Dec. 20, 2005,
and to issue a final rule by Sept. 27, 2006.

That rule may, or may not,
include changes to the existing standards.
EPA estimates that meeting existing PM 2.5 standards will prevent at
least:15,000 premature deaths; 75,000 cases of chronic bronchitis;
10,000 hospital admissions for respiratory and cardiovascular disease;
hundreds of thousands of occurrences of aggravated asthma; and 3.1
million days when people miss work because they are suffering from
symptoms related to particle pollution exposure.
The reduction of fine particle pollution is a critical element of the
Administration's comprehensive national clean air strategy. The
strategy includes EPA's recent Clean Diesel Program to reduce pollution
from highway, nonroad and stationary diesel engines, the Clean Air
Interstate Rule to reduce pollution from power plants in the eastern
United States, and the Clean Air Visibility Rule.

To read the final staff paper, a fact sheet, and related materials, go
to:
http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_index.html

To read
the CASAC letter to the Administrator regarding the previous draft of
the staff paper, go to:

http://www.epa.gov/sab/pdf/casac-05-007.pdf

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5.3.7 Summary of Staff Recommendations on Primary PM2.5 NAAQS

Staff recommendations for the Administrator's consideration in making decisions on the
primary PM2.5 standards, together with supporting conclusions from sections 5.3.1 through 5.3.6,
are briefly summarized below...

( 1) Consideration should be given to revising the current PM2.5 primary standards to provide
increased public health protection from the effects of both long- and short-term exposures
to fine particles in the ambient air. This recommendation is based in general on the
evaluation in the CD of the newly available epidemiologic, toxicologic, dosimetric, and
exposure-related evidence, and more specifically on the evidence of mortality and
morbidity effects in areas where the current standards were met, together with judgments
as to the public health significance of the estimated incidence of effects upon just
attaining the current standards.
( 2) The indicator for fine particle standards should continue to be PM2.5. This
recommendation is based on the conclusion that the available evidence does not provide
a sufficient basis for replacing or supplementing a mass-based fine particle indicator with
an indicator for any specific fine particle component or subset of fine particles, nor does
it provide a basis for excluding any components; on the evaluation in the CD of air
quality within the intermodal particle size range of 1 to 3 µm; and on the policy judgment
made in the last review to place regulatory importance on defining an indicator that
would more completely capture fine particles under all conditions likely to be
encountered across the U.S., while recognizing that some limited intrusion of small
coarse particles will occur in some circumstances. Consideration should be given to
modifying the FRM for PM2.5 based on instrumentation and operational improvements
that have been made since the PM2.5 monitoring network was deployed in 1999, and to
the adoption of FEMs for appropriate continuous measurement methods.
( 3) Averaging times for PM2.5 standards should continue to include annual and 24-hour
averages to protect against health effects associated with short-term (hours to days) and
long-term (seasons to years) exposure periods. Consideration of other averaging times,
especially on the order of one or more hours, was limited by a lack of adequate
information at this time.
( a) Consideration should be given to revising the form of the annual standard to one
based on the highest community-oriented monitor in an area or, alternatively, to
one with more constrained requirements for the use of spatial averaging across
community-oriented monitors.
( b) Consideration should be given to revising the form of the 24-hour standard to a
99th percentile form or, alternatively, to retaining the 98th percentile form, based in
part on considering the degree of risk reduction likely to result from the
combination of the form and the level of a standard.
( 4) Consideration should be given to alternative suites of PM2.5 standards to provide
protection against effects associated with both long- and short-term exposures, taking
into account both evidence-based and risk-based considerations. Integrated
recommendations on ranges of alternative suites of standards that, when considered
together, protect against effects associated with both long- and short-term exposures
include:
( a) Staff recommends consideration of an annual PM2.5 standard at the current level
of 15 µg/m3 together with a revised 24-hour PM2.5 standard in the range of 35 to
25 µg/m3, based a 98th percentile form for a standard set at the middle to lower
end of this range, or a 99th percentile form for a standard set at the middle to upper
end of this range. Staff judges that such a suite of standards could provide an
appropriate degree of protection against serious mortality and morbidity effects
associated with long- and short-term exposures to fine particles.
( b) Alternatively, staff also recommends consideration of a revised annual PM2.5
standard, within the range of 14 to 12 µg/m3, together with a revised 24-hour
PM2.5 standard in the range of 30 to 40 µg/m3.