Dan Campbell, a member of USA Today's Board of contributors and a long-time Washington Post correspondent, penned an article for USA Today yesterday entitled "Demand more funding for Alzheimer's." It pictured singer Glen Campbell (related?) along with twenty column inches of text.
Campbell has found similar disconnects in the system to our findings re COPD research. For example:
From 2000 to 2010, the percentage of deaths in the U.S. from cancer, HIV/AIDs and cardiovascular diseases declined, some sharply, while deaths of people with Alzheimer's skyrocketed. The numbers reflect the money spent by the National Institutes of Health on research. For example, this year NIH is spending nearly seven times as much on HIV/AIDs as it is on Alzheimber's, though there are five times as many people with Alzheimer's as with HIV/AIDS. This ratio 35 to 1, is shocking, but sadly true.
Campbell comes at the issue several ways -- the costs in the system, an aging bias in the research community (4% of Americans < 65 afflicted, almost 50% over 65 afflicted). I don't buy this particular statistic -- it probably should be 'almost 50% of those over 65 will show symptoms at some point' which is very different, and doesn't mean that half of us will inevitable drool for many years while gibbering. Nonetheless, the point is clear -- this is a frightening and debilitating disease that is hugely underfunded.
I love Campbell's closing idea -- demand that their U.S. representatives and senators spend one hour, without aides or professional escorts, wandering around an advanced-staage Alzheimer's ward. Not only would that quickly loosen federal purse strings for Alzheimer's research, those purse strings would virtually disappear. Guaranteed.
That is a great idea, and having tended for an aging parent severely afflicted by this horrible disease, I applaud the idea. However, I am not so sanguine as to think Congress would act. They cannot get their minds around gun control, or a million other topics -- this one seems equally elusive.
But, let's hope that a fire could be lit. And if it burns a little brightly, maybe COPD, which kils three times as many and has one-third the research money of Alzheimer's, might also be given more hope.
Wednesday, September 18, 2013
Sunday, August 25, 2013
COPD in a TEDx talk
I couldn't resist inserting a few slides into this TED talk about Innovation Resilience
http://www.youtube.com/watch?v=a2oeSFkV7eE&feature=youtu.be
The pertinent time is between 13:00 and 15:05 minutes
http://www.youtube.com/watch?v=a2oeSFkV7eE&feature=youtu.be
The pertinent time is between 13:00 and 15:05 minutes
Progress on the hypothesis
Discussions recently with several universities about our COPD thesis have uncovered some surprising support, but not where I would have expected it. Instead of Medical Schools, or even Public Health schools, the groups that have surfaced are (1) Computer Graphics and Big Data schools who have GIS (Graphical Informations Systems) experience; and (2) nanotechnology departments (of which there are not very many).
The latter has really surprised me, until they explained that the craze about 3-D printers is causing some consternation. These fabulous tools (mostly invented at HP some twenty years ago, but now the patents have run out) spray ultra-fine particies by definition, to construct the products of interest.
Lots of materials qualify to be "sprayed" or deposited, including the possibility of pretty toxic material. All of a sudden, there is renewed interest in industrial air contamination. Which led them to our thesis.
Amazing bed fellows in a long journey...
The latter has really surprised me, until they explained that the craze about 3-D printers is causing some consternation. These fabulous tools (mostly invented at HP some twenty years ago, but now the patents have run out) spray ultra-fine particies by definition, to construct the products of interest.
Lots of materials qualify to be "sprayed" or deposited, including the possibility of pretty toxic material. All of a sudden, there is renewed interest in industrial air contamination. Which led them to our thesis.
Amazing bed fellows in a long journey...
Saturday, June 15, 2013
The Verdict?
The O J Simpson murder trial produced some strange evidence that proved insufficient to find him guilty -- a DNA smear attributable to one person in ten million put him at the scene of the murders; a shrunken leather glove that did not easily go on his hand was exonerating. And the jury, not steeped in DNA testing in 1995, acquited!
So here we are with COPD, and the evidenciary trail with fine particulate matter and its implication in toxic gaseous atmospheres for COPD is strong, evidence based on measurements by multiple independent groups using a variety of methods, since 1970. The most indicting date back to 1974, with methods that have been rehashed, reanalyzed, and even duplicated by multiple other teams, with nearly identical findings over and over. These results have been published in respectable medical journals and through independent agencies starting twenty years ago. They have been the basis of EPA regulations for over a decade. The debate, once vociferous, has dwindled.
Yet the AMA stance remains totally dedicated to the statement that "COPD is a smoker's disease".
This AMA frozen position is one of the best examples of paradigm rigidity as described by Thomas Kuhn, who said in The Structure of Scientific Revolutions:
A) "There is no standard higher than the assent of the relevant community..., this issue of paradigm choice can never be unequivocally settled by logic and experiment alone."
B) "The usual prelude (to a paradigm shift) ... is the awareness of anomaly, of an occurrence or set of occurrences that does not fit existing ways of ordering phenomena. The changes that result therefore require 'putting on a different kind of thinking cap', one that renders the anomalous law like, but that in the process also transforms the order exhibited by some other phenomena, previously unproblematic."
Kuhn pointed out Max Planck's apt observation: "a new scientific truth does not triumph by convincing its opponents and making them see the light, but rather because its opponents eventually die, and a new generation grows up that is familiar with it."
Perhaps, then, we can hope that the next generation will begin to assess these additional important causes of COPD, which could even (gasp) lead to research into the emissions of those elements (as though we didn't know that it is mostly fossil-fuel power plants and automotive exhausts), and that in turn could lead to more effective emission controls, or power source changes, and hopefully to more effective treatments. Whew... lots still to do.
So here we are with COPD, and the evidenciary trail with fine particulate matter and its implication in toxic gaseous atmospheres for COPD is strong, evidence based on measurements by multiple independent groups using a variety of methods, since 1970. The most indicting date back to 1974, with methods that have been rehashed, reanalyzed, and even duplicated by multiple other teams, with nearly identical findings over and over. These results have been published in respectable medical journals and through independent agencies starting twenty years ago. They have been the basis of EPA regulations for over a decade. The debate, once vociferous, has dwindled.
Yet the AMA stance remains totally dedicated to the statement that "COPD is a smoker's disease".
This AMA frozen position is one of the best examples of paradigm rigidity as described by Thomas Kuhn, who said in The Structure of Scientific Revolutions:
A) "There is no standard higher than the assent of the relevant community..., this issue of paradigm choice can never be unequivocally settled by logic and experiment alone."
B) "The usual prelude (to a paradigm shift) ... is the awareness of anomaly, of an occurrence or set of occurrences that does not fit existing ways of ordering phenomena. The changes that result therefore require 'putting on a different kind of thinking cap', one that renders the anomalous law like, but that in the process also transforms the order exhibited by some other phenomena, previously unproblematic."
Kuhn pointed out Max Planck's apt observation: "a new scientific truth does not triumph by convincing its opponents and making them see the light, but rather because its opponents eventually die, and a new generation grows up that is familiar with it."
Perhaps, then, we can hope that the next generation will begin to assess these additional important causes of COPD, which could even (gasp) lead to research into the emissions of those elements (as though we didn't know that it is mostly fossil-fuel power plants and automotive exhausts), and that in turn could lead to more effective emission controls, or power source changes, and hopefully to more effective treatments. Whew... lots still to do.
Friday, June 14, 2013
Further research studies
In the May 11 post ("Digging deeper into COPD by locale", I mentioned the Dockery, Pope, and et al paper of 1993, suggesting that it "should have been widely acknowledged, and galvanizing." In fact, it was, so much so that it both stimulated EPA to consider tough new emission regulations for power plants and air pollution measurements, and a series of critiques and re-assessments of the research itself.
Pope, an economist now at BYU, and Dockery, still at Harvard, have continued work in this area, publishing a key ACS 1995 follow-on paper (also cited in my May 11 post) considering 151 additional cities, and a 2009 study re life expectancy if pollution levels are reduced.
But the fun ones are as follows:
A) "Air Pollution and Mortality," S.H. Moolgavkar, Fort Hutchinson Cancer Research Center in Seattle, WA, published in correspondence w New England Journal of Medicine, April 28, 1994, 330:1237-1238 with a rebuttal by Dockery and Pope. Moolgavkar did a great deal of classic nit-picking, partially around the 5-year groupings for age-adjustments, and failure fully to include socioeconomic and occupational exposures. This lament precedes the next entry.
B) "A critical review of the evidence on particulate air pollution and mortality", S.H. Moolgavkar and E.G. Luebeck, at the Fort Hutchinson Cancer Research Center in Seattle, WA, published in Epidemiology, July 1996 (7(4), 420-8. They conclude "it is not possible with the present evidence to show a convincing correlation between particulate air pollution and mortality."
C) "Reanalysis of the Harvard Six Cities Study and the American Cancer Society Study of Particulate Air Pollution and Mortality," Daniel Krewski, Richard Burnett and et al, The Health Effects Insitute, July 2000. From the opening statement of the 200+ page report: "Both of these studies came under intense scrutiny in 1997 when the EPA used the results to support new National Ambient Air Quality Standards for fine particles and to maintain the standards for particles less than 10 μm in median aerodynamic diameter (PM10) already in effect. Members of Congress and industry, the scientific community and others interested in regulation of air quality scrutinized the studies’ methods and their results. Some insisted that any data generated using federal funding should be made public. Others argued that these data had been gathered with assurances of confidentiality for the individuals who had agreed to participate and that the concept of public access to federally funded data did not take into account the intellectual property rights of the investigators and their supporting institutions. To address the public controversy, Harvard University and the ACS requested that the Health Effects Institute organize an independent reanalysis of the data from these studies. Both institutions agreed to provide access to their data to a team of analysts to be selected by HEI through a competitive process." The reanalysis was quite supportive of the data, methodology, and conclusions, while adding some ideas for further work.
D) "Fine Particulate air pollution and mortality in 20 U.S. Cities, 1987-1994," J.M. Sarnat et al, Dept of Epidemiology et al, Johns Hopkins University, published in New England Journal of Medicine, Dec. 14, 2000, 343 (24): 1742-9. This study found that: "there is consistent evidence that the levels of fine particulate matter in the air are associated with the risk of death from all cause and from cardiovascular and respiratory illnesses. These findings strengthen the rationale for controlling the levels of respirable particles in outdoor air." This article drew comment from J.H.Ware, pp. 1798-99. and a follow-up by Sarnat et al, NEJM, Apr 19, 2001; 344 (16), 1253-54. Ware was one of the Dockery et al authors.
E) "Overview of the re-analysis of the Harvard Six Cities Study and American Cancer Society (ACS) study of Particulate Air Pollution and Mortality," D. Krewski, et al, at the McLaughlin Center for Population Health Risk Assessment, Ottawa, Canada, published in the Journal of Toxicology and Environmental Health, Aug 22, 2003 and Oct 10, 2003; 66 (16, 19): 1507-51. They conclude that the data and the methods support: "the reported association for fine particles mortality of the original investigators as well as demonstrating a significant association between sulfur dioxide and mortality. Collectively, our re-analysis suggest that mortality may be attributable to more than one component of the complex mixture of ambient air pollutants in U.S. urban areas."
F) "Mortality and long-term exposure to ambient air pollution" D. Krewski et al, at the McLaughlin Center for Population Health Risk Assessment, Ottawa, Canada, published in the Journal of Toxicology and Environmental Health, Jul 9 & 23, 2005; 68 (13, 14): 1093-1109. This article describes on-going work to explore the role of ecologic, economic, and demographic covariates in the particulate air pollution and mortality association.
G) "Extended follow-up and spatial analysis of the ACS study linking particulate air pollution and mortality," D. Krewski et al, at the McLaughlin Center for Population Health Risk Assessment, Ottawa, Canada, published as a Research Report of the Health Effects Institute, May 2009 (140)5-114, discussion 115-36. This work was extensive, and concluded that there was significant (+7.5% and +12.8%) mortality effects from ischemic heart disease and cardiopulmonary disease especially, linked to simultaneous exposure to sulfur dioxides and PM2.5 particulates. In Los Angeles, the spatial analysis showed air-pollution mortality ratios 3x higher than previously reported. No significant correlations were found in New York City.
Pope, an economist now at BYU, and Dockery, still at Harvard, have continued work in this area, publishing a key ACS 1995 follow-on paper (also cited in my May 11 post) considering 151 additional cities, and a 2009 study re life expectancy if pollution levels are reduced.
But the fun ones are as follows:
A) "Air Pollution and Mortality," S.H. Moolgavkar, Fort Hutchinson Cancer Research Center in Seattle, WA, published in correspondence w New England Journal of Medicine, April 28, 1994, 330:1237-1238 with a rebuttal by Dockery and Pope. Moolgavkar did a great deal of classic nit-picking, partially around the 5-year groupings for age-adjustments, and failure fully to include socioeconomic and occupational exposures. This lament precedes the next entry.
B) "A critical review of the evidence on particulate air pollution and mortality", S.H. Moolgavkar and E.G. Luebeck, at the Fort Hutchinson Cancer Research Center in Seattle, WA, published in Epidemiology, July 1996 (7(4), 420-8. They conclude "it is not possible with the present evidence to show a convincing correlation between particulate air pollution and mortality."
C) "Reanalysis of the Harvard Six Cities Study and the American Cancer Society Study of Particulate Air Pollution and Mortality," Daniel Krewski, Richard Burnett and et al, The Health Effects Insitute, July 2000. From the opening statement of the 200+ page report: "Both of these studies came under intense scrutiny in 1997 when the EPA used the results to support new National Ambient Air Quality Standards for fine particles and to maintain the standards for particles less than 10 μm in median aerodynamic diameter (PM10) already in effect. Members of Congress and industry, the scientific community and others interested in regulation of air quality scrutinized the studies’ methods and their results. Some insisted that any data generated using federal funding should be made public. Others argued that these data had been gathered with assurances of confidentiality for the individuals who had agreed to participate and that the concept of public access to federally funded data did not take into account the intellectual property rights of the investigators and their supporting institutions. To address the public controversy, Harvard University and the ACS requested that the Health Effects Institute organize an independent reanalysis of the data from these studies. Both institutions agreed to provide access to their data to a team of analysts to be selected by HEI through a competitive process." The reanalysis was quite supportive of the data, methodology, and conclusions, while adding some ideas for further work.
E) "Overview of the re-analysis of the Harvard Six Cities Study and American Cancer Society (ACS) study of Particulate Air Pollution and Mortality," D. Krewski, et al, at the McLaughlin Center for Population Health Risk Assessment, Ottawa, Canada, published in the Journal of Toxicology and Environmental Health, Aug 22, 2003 and Oct 10, 2003; 66 (16, 19): 1507-51. They conclude that the data and the methods support: "the reported association for fine particles mortality of the original investigators as well as demonstrating a significant association between sulfur dioxide and mortality. Collectively, our re-analysis suggest that mortality may be attributable to more than one component of the complex mixture of ambient air pollutants in U.S. urban areas."
F) "Mortality and long-term exposure to ambient air pollution" D. Krewski et al, at the McLaughlin Center for Population Health Risk Assessment, Ottawa, Canada, published in the Journal of Toxicology and Environmental Health, Jul 9 & 23, 2005; 68 (13, 14): 1093-1109. This article describes on-going work to explore the role of ecologic, economic, and demographic covariates in the particulate air pollution and mortality association.
G) "Extended follow-up and spatial analysis of the ACS study linking particulate air pollution and mortality," D. Krewski et al, at the McLaughlin Center for Population Health Risk Assessment, Ottawa, Canada, published as a Research Report of the Health Effects Institute, May 2009 (140)5-114, discussion 115-36. This work was extensive, and concluded that there was significant (+7.5% and +12.8%) mortality effects from ischemic heart disease and cardiopulmonary disease especially, linked to simultaneous exposure to sulfur dioxides and PM2.5 particulates. In Los Angeles, the spatial analysis showed air-pollution mortality ratios 3x higher than previously reported. No significant correlations were found in New York City.
Monday, May 20, 2013
The suggestive evidence
COPD observations and studies
Data
supporting the assertion that smoking is not the only (maybe not even the
primary) cause of COPD comes from five separate categories of observations:
1. The demographic disparity between locales of
smoking prevalence and COPD death-rates, whether shown by comparisons of the
fifty states, the 805 Health Service Areas, or the county-by-county
examinations of a few states (two Colorado studies were briefly described
herein).
2. Examination of specific emphysema death records for
a decade in Colorado, which did not reveal significant correlation with
long-term smoking habits.
3. Anecdotal evidence from numerous hospice nurses
that they have attended many patients who died of COPD who had never smoked.
4. The uncommon (but not rare) genetic disorder Alpha-1
COPD has nothing to do with smoking – it affects an estimated 100,000 persons
in America, three times more than Cystic Fibrosis for example, and is virtually
untreatable. It is but one rare form of COPD, but one that makes a victim
'crazy' with the notion that 'most people who get COPD deserve it' as the New
York Times story about Johnny Carson's death phrased it.
Sally
Everett has written a book "Alpha 1
COPD, A Love Story" available at Amazon, and a blog about her
experiences and findings. See the chilling post
at http://curecopd.blogspot.com/2012/01/real-silent-killer.html.
5. Recent research into ultra-fine particle impacts,
to which we now turn:
COPD
ultra-fine particulate studies
Data supporting the sub-micron particulate
thesis as a possible causal agent for asthma has been mounting for two
decades. In 1993, scientists with
a National Institutes of Health grant released a study of the impact of small
particulate matter – in their case, particles smaller than 2.5 microns (known
as PM2.5) – in six “cities”, showing quite significant correlation
with COPD and asthmatic incidence. [1] The cities were, for the most part, small
rural towns, studied for a twenty year period, isolating the effect of air
pollution on control samples of both smokers and non-smokers. The conclusion was that there was fifty
percent higher correlation with small particulates (less than 2.5 microns) than
from smoking for COPD incidence.
In 1995, a longitudinal study of 552,138 individuals in 151 cities found that:
Particulate
air pollution was associated with cardiopulmonary and lung cancer mortality but
not with mortality due to other causes. Increased mortality is associated with
sulfate and fine particulate air pollution at levels commonly found in U.S.
cities. The increase in risk is not attributable to tobacco smoking, although
other unmeasured correlates of pollution cannot be excluded with certainty.[2]
A 2009 study by the same researchers correlates pollution and life expectancy:
We compiled data on
life expectancy, socioeconomic status, and demographic characteristics for 211
county units in the 51 U.S. metropolitan areas with matching data on
fine-particulate air pollution for the late 1970s and early 1980s and the late
1990s and early 2000s. Regression models were used to estimate the association
between reductions in pollution and changes in life expectancy, with adjustment
for changes in socioeconomic and demographic variables and in proxy indicators
for the prevalence of cigarette smoking.
A reduction in exposure to ambient fine-particulate air pollution contributed to significant and measurable improvements in life expectancy in the United States. [3]
Recent studies have taken this work deeper. Consider these 2013 findings at U C Davis:
Scientists
at the University of California, Davis, have, for the first time, developed a
system that can determine which types of air particles that pollute the
atmosphere are the most prevalent and toxic.
Previous
research has shown that air pollution containing fine and ultrafine particles
is associated with asthma, heart disease and premature death. This new study,
released today by the California Air Resources Board and the Electric Power
Research Institute, marks the first time that researchers have conducted source-oriented
sampling of these particles in the atmosphere.
For example, the researchers found that particulate emissions from vehicles, wood burning and residential cooking exhibited the most toxic effects at the study site in Fresno, which has among the nation’s highest rates of adult and childhood asthma.
“Right now, air quality standards are based on the mass of particulate matter and don’t distinguish between natural sources, like sea spray, and known toxic sources, like diesel exhaust,” said Anthony Wexler, the principal investigator and director of the Air Quality Research Center at UC Davis. “This study will help regulators control only the sources that are toxic, which saves money.”
The researchers used a single particle mass spectrometer, co-developed by Wexler, and 10 particle samplers to collect, analyze and separate ambient particles.
Laboratory mice then inhaled particle samples from the separate sources. Kent Pinkerton, a professor of pediatrics at the UC Davis School of Medicine, monitored their responses for signs of toxicity.
“This demonstrates that particles of different sources have different degrees and kinds of toxicity,” said Pinkerton. “We need to use this information to better understand the health effects of particulate matter. If we don’t, we’ll never really come up with a solution.” [4]
A 2009 study in New Orleans is
particularly intriguing for studying the early age impact:
Stephania Cormier, PhD, Associate Professor of
Pharmacology at LSU Health Sciences Center New Orleans, has shown for the first
time that early exposure to environmentally persistent free radicals (present
in airborne ultrafine particulate matter) affects long-term lung function. She
recently presented her latest research data at the 11th International Congress on
Combustion By-Products and Their Health Effects at the Environmental Protection
Agency Conference Center in Research Triangle Park, N.C.
Using protein profiling techniques, Dr. Cormier’s lab was able to determine that early exposure to these ultrafine pollutants caused genes to produce a number of proteins, including one associated with COPD and steroid-resistant asthma, and also caused proteins to misfold, rendering them dysfunctional. These genetic defects are linked to structural changes in the lung, airflow limitations, and permanent changes in immune responses.
“It is no surprise that elevations in airborne particulate matter (PM) are associated with increased hospital admissions for respiratory symptoms including asthma exacerbations,” notes Dr. Cormier.
“What has come as a surprise is that early exposure to elevated levels of PM elicits long-term effects on lung function and lung development in children.”
These results could be especially important because the US Environmental Protection Agency does not currently regulate ultrafine PM emissions.[5]
Others are now deciding to weigh in. Here’s an April 13, 2013 report from Rice University:
Rice University and the University of Houston will collaborate in a study to determine how
and where air quality in Houston affects the health of residents. Researchers will roam the streets in Houston
over the course of two years and use a mobile lab to collect data on air
pollutants smaller than 2.5 micrometers. Particles smaller than 10 micrometers
can get into the lungs and blood stream and affect a person's heart. In addition, researchers will determine which
neighborhoods in the city are at higher risk from those small particles, as a
result of traffic or industry…. The
study is funded by the Houston Endowment. [6]
The European Center for Energy, Environment, and Health (CEEH) produced a lengthy report in 2011, reviewing much pertinent literature, including Dockery and Pope papers, concluding that there is a clear connection between an increase in fine particulate matter (PM2.5) and the following four diseases: coronary heart disease (CHD), stroke, chronic obstructive pulmonary disease (COPD), and lung cancer [7]
SEEMS REMARKABLE WITH ALL OF THIS "EVIDENCE" that the AMA still resists believing that there is more to all of this than SMOKING
[1] Douglas Dockery, C. Arden Pope III, Xiping Xu, John D.
Spengler, James H. Ware, Martha E. Fay, Enjamin G. Ferris, Jr.; and Frank E.
Speizer, “An Association between Air Pollution and Mortality in Six U.S.
Cities,” New England Journal of Medicine (329: 24), December 9, 1993, pp. 1753-59
[2] Pope, CA, III; Thun, MJ; Namboodiri, MM; Dockery, DW;
Evans, JS; Speizer, FE; Heath, CW, Jr; : Particulate air pollution as a
predictor of mortality in a prospective study of US adults ,”
American Journal of Respiratory and Critical Care Medicine (3:1), pp.
669-674.
3] C. Arden Pope,
III, Ph.D., Majid Ezzati, Ph.D., and Douglas W. Dockery, Sc.D.; “Fine-Particulate
Air Pollution and Life Expectancy in the United States,” New England
Journal of Medicine, 2009; 360:376-386, January 22, 2009
[4] Ken Kerlin, “Scientists trace particulate air
pollution to its source.” UC
Davis News Service, February
19, 2013. The California Air
Resources Board and the Electric Power Research Institute (EPRI) funded the
study.
[5] “Infant Inhalation Of Ultrafine Air Pollution Linked To Adult Lung Disease,” Louisiana State University Health Sciences Center, July 23 2009; http://www.sciencedaily.com/releases/2009/07/090722123751.htm
[6] Bayan Raji, “Rice, UH to study how air pollution
impacts Houstonians,” Houston Business
Journal, April 24, 2013
[7] See CEEH Scientific Report 7a, “Description of the CEEH
health effects model – selection of concentration-response functions; “ http://www.ceeh.dk/CEEH_Reports/Report_7a/CEEH_Report_7a.pdf
The PROPOSAL
The Problem
COPD
death-rate statistics by state and by local region (county or Health Service
Area) within states have been available for many years. But even with age-adjusted data shifts, they
do not correlate very well with smoker prevalence or lung cancer death rates by
locale. Nor do they correlate with
contaminated urban air pollution levels, long monitored by state air pollution
agencies. This problem, though well
recognized, has not generated significant study by CDC, AMA, or the American
Lung Association. Unfortunately, the AMA stance is
unquestioned, to the point that it has stifled research into both cause and
treatment for fifty years for a massively expensive, debilitating disease. In those fifty years, five million Americans
have died from COPD, and an additional five million have died where COPD was
the secondary disease that triggered the primary death from heart attack or
stroke.
A hypothesis
A few
scholarly studies have pinpointed fine-grain particulate material (smaller than 2.5
microns, usually written as PM2.5) as a potential source of airway insult, correlating local measurements
with increased COPD death-rates independent of smoking. Fine-grain particulates, combined with toxic
molecules in a ground-hugging atmosphere, could be possible agents for
ingestion into the lung, with sufficient retention to cause significant spot
damage. Such agents might be causal for
long-term lung damage, analogous to asbestosis.
Coal-fired power plants are a
primary producer of sub-micron fly ash particulate; such emissions are hard
both to measure and control with current technology. Moreover, coal-fired power plants have
increased their output by 240% in the past thirty years across America, as have
cars with toxic gases.
A proposal
Ten
million deaths in fifty years, examined from a ‘big data’ correlation analysis
viewpoint, could potentially yield significant new information as to cause and
possible mitigation. An InnovaScapes
Institute research proposal is in preparation in order to stimulate wider
inquiry and appropriate action.
Saturday, May 11, 2013
Digging deeper into COPD by locale
Three remarkable studies in recent years go deeper into COPD locales:
The first of these was a study of six relatively small towns, from 1974-1990, conducted by seven doctors and reported in the New England Journal of Medicine in 1993. This was the first study with control groups to 'null out' the effect of smoking. The results were striking; very fine particulate material (2.5 microns and below) were implicated at a 50% higher rate than any other contaminant -- in such towns as Portage, WI (population 10,000); Watertown, MA (32,000); Harriman, TN (pop. 6000); Topeka, KS (127,000); a portion of St. Louis (half? of 320,000), and Steubenville, OH (19,000). This study should have been widely acknowledged, and galvanizing.
[1] Douglas Dockery, C. Arden Pope III, Xiping Xu, John D. Spengler, James H. Ware, Martha E. Fay, Enjamin G. Ferris, Jr.; and Frank E. Speizer, “An Association between Air Pollution and Mortality in Six U.S. Cities,” New England Journal of Medicine (329: 24), December 9, 1993
The second of these was done by three CDC statisticians, reporting CDC COPD death-rates by HSA (Health-Service Area), which is 805 separate health areas for America (versus 50 states, and 3,000+ counties). Colorado, for example, is granular of ONE as a state; 64 as counties, and 16 HSA regions (four of which are shared across state boundaries). They studied five-year aggregated age-normalized COPD death-rates for three periods ('83-'87; '88-'92; and '93-'97), along with a map of 'hot spots' for change in ranking (Figure 5 counting from the last post). The Rockies and New England were stunningly high in COPD death-rates; the South with its high smoking prevalence was low. Again, so far as I know, this important 2001 paper received almost no acknowledgment.
The final paper that I will mention along these lines was commissioned by the Colorado COPD Institute, to study deeper why Colorado is consistently among the top COPD death-rate states, even though it is not a high-smoking state. While it found not 'smoking gun', it was suggestive, and it certainly comfirmed that urban areas were not high in incidence.
[3] Ryan McGhan and Greg Kinney, “2007 Colorado Chronic obstructive pulmonary disease (COPD) Surveillance Report”, Colorado COPD Institute, with the American Lung Association, Colorado branch
The first of these was a study of six relatively small towns, from 1974-1990, conducted by seven doctors and reported in the New England Journal of Medicine in 1993. This was the first study with control groups to 'null out' the effect of smoking. The results were striking; very fine particulate material (2.5 microns and below) were implicated at a 50% higher rate than any other contaminant -- in such towns as Portage, WI (population 10,000); Watertown, MA (32,000); Harriman, TN (pop. 6000); Topeka, KS (127,000); a portion of St. Louis (half? of 320,000), and Steubenville, OH (19,000). This study should have been widely acknowledged, and galvanizing.
[1] Douglas Dockery, C. Arden Pope III, Xiping Xu, John D. Spengler, James H. Ware, Martha E. Fay, Enjamin G. Ferris, Jr.; and Frank E. Speizer, “An Association between Air Pollution and Mortality in Six U.S. Cities,” New England Journal of Medicine (329: 24), December 9, 1993
The second of these was done by three CDC statisticians, reporting CDC COPD death-rates by HSA (Health-Service Area), which is 805 separate health areas for America (versus 50 states, and 3,000+ counties). Colorado, for example, is granular of ONE as a state; 64 as counties, and 16 HSA regions (four of which are shared across state boundaries). They studied five-year aggregated age-normalized COPD death-rates for three periods ('83-'87; '88-'92; and '93-'97), along with a map of 'hot spots' for change in ranking (Figure 5 counting from the last post). The Rockies and New England were stunningly high in COPD death-rates; the South with its high smoking prevalence was low. Again, so far as I know, this important 2001 paper received almost no acknowledgment.
[2] Jay H. Kim, Jimmie D. Givens, Jai W. Choi; “Geographic
Distribution and Changes in COPD Mortality: United States, 1983-1997, National
Center for Health Statistics, Hyattsville, MD, presented at American
Statistical Society, August, 2001.
The final paper that I will mention along these lines was commissioned by the Colorado COPD Institute, to study deeper why Colorado is consistently among the top COPD death-rate states, even though it is not a high-smoking state. While it found not 'smoking gun', it was suggestive, and it certainly comfirmed that urban areas were not high in incidence.
[3] Ryan McGhan and Greg Kinney, “2007 Colorado Chronic obstructive pulmonary disease (COPD) Surveillance Report”, Colorado COPD Institute, with the American Lung Association, Colorado branch
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