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 PM_2.5) – 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 (PM_2.5) 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

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[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 PM_2.5) 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. 

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.

[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