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.
Saturday, June 15, 2013
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.
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