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From: (Sol Lightman)
Newsgroups: alt.drugs
Subject: Lung Cancer MJ/Tobacco
Date: 5 May 1993 05:25:54 GMT
Message-ID: <1s7j52$>

|A thank you to Lamont Granquist (sp?) who origionally posted this
|article.  I dug up the remaining letters and typed them in.

|Just to keep things straight
|(-- This is me

This is the quoted article.

Winters-TH, Franza-JR, Radioactivity in Cigarette Smoke, 
New England Journal of Medicine, 1982; 
306(6): 364-365  (reproduced w/o permission)

  To the Editor:  During the 17 years since the Surgeon General's
first report on smoking, intense research activity has been focused
on the carcinogenic potential of the tar component of cigarette
smoke.  Only one definite chemical carcinogen -- benzopyrene --

|see correction in follow-up letters, many other identified
|chemical carcinogens are present.  The question is, what is their
|relative risk compared with the "radioelements''

has been found.  Conspicuous because of its absence is research into
the role of the radioactive component of cigarette smoke.
  The alpha emitters polonium-210 and lead-210 are highly con-
centrated on tobacco trichomes and insoluble particles in cigarette
smoke (1).  The major source of the polonium is phosphate fertilizer,
which is used in growing tobacco.  The trichomes of the leaves con-
centrate the polonium, which persists when tobacco is dried and
  Levels of Po-210 were measured in cigarette smoke by Radford and
Hunt (2) and in the bronchial epithelium of smokers and nonsmokers
by Little et al. (3)  After inhalation, ciliary action causes the insoluble
radioactive particles to accumulate at the bifurcation of segmental
bronchi, a common site of origin of bronchogenic carcinomas. 
  In a person smoking 1 1/2 packs of cigarettes per day, the radia-
tion dose to the bronchial epithelium in areas of bifurcation is 8000
mrem per year -- the equivalent of the dose to the skin from 300
x-ray films of the chest per year.  This figure is comparable to total-
body exposure to natural background radiation containing 80
mrem per year in someone living in the Boston area.
  It is a common practive to assume that the exposure received
from a radiation source is distributed throughout a tissue.  In this
way, a high level of exposure in a localized region -- e.g. bronchial
epithelium -- is averaged out over the entire tissue mass, suggest-
ing a low level of exposure.  However, alpha particles have a range of
only 40 um in the body.  A cell nucleus of 5 to 6 um that is traversed
by a single alpha particle receives a dose of 1000 rems.  Thus, although
the total tissue dose might be considered negligible, cells
close to an alpha source receive high doses.  The Po-210 alpha activity
of cigarette smoke may be a very effective carcinogen if a multiple
mutation mechanism is involved.
  Radford and Hunt have determined that 75 per cent of the alpha 
activity of cigarette smoke enters the ambient air and is unab-
sorbed by the smoker, (2) making it available for deposit in the lungs
of others.  Little et al. have measured levels of Po-210 in the lungs of
nonsmokers that may not be accounted for on the basis of natural
exposure to this isotope.
  The detrimental effects of tobacco smoke have been considerably
underestimated, making it less likely that chemical carcinogens
alone are responsible for the observed incidence of tobacco-related
carcinoma.  Alpha emitters in cigarette smoke result in appreciable
radiation exposure to the bronchial epithelium of smokers and
probably secondhand smokers.  Alpha radiation is a possible etio-
logic factor in tobacco-related carcinoma, and it deserves further

                                          Thomas H. Winters, M.D.
                                        Joseph R. Di Franza, M.D.
                                      University of Massachusetts
Worcester, Ma 01605                                Medical Center

1.  Martell EA. Radioactivity of tobacco trichomes and insoluble cigarette
    smoke particles.  Nature.  1974; 249:215-7.
2.  Radford EP Jr, Hunt VR.  Polonium-210: a volatile radioelement in cig-
    arettes.  Science.  1964; 143:247-9
3.  Little JB, Radford EP Jr, McCombs HL, Hunt VR.  Distribution of po-
    lonium-210 in pulmonary tissues of cigarette smokers.  N Engl J Med.
    1965; 273:1343-51.

Responses to this letter:

NEJM 307(5):309-313.  reproduced w/o permission

  To the Editor:  In a letter in the Feb 11 issue, Winters and DiFranza (1)
correctly point out that alpha radiation from polonium-210 is a possible
causal factor in tobacco-related carcinoma, but they incorrectly state that
"inhaled'' Po210 is a factor and that research on this important possibility 
has been neglected.  I will briefly review recent pertinent research.
  Radford and Hunt (2) first suggested that alpha radiation from Po210 in
cigarette smoke may be important in the genesis of bronchial cancer.  Little
et al. (3) found surprisingly high concentrations of Po210 at single bronchial
bifurcations in seven of 37 cigarette smokers.  Holtzman and others (4 - 6)
raised doubts about the validity of these observations because inhaled 
volatile Po210 is soluble and rapidly cleared.  Subsequently, I determined (7)
that lead-210 (a beta-emitting precursor of Po210) is highly concentrated 
in tobacco trichomes and that trichome combustion in burning cigarettes 
produces insoluble, Pb210-enriched particles in mainstream smoke.  Thus, the
high concentrations of Po210 observed at segmental bifurcations (4 - 6) can
be explained by the persistence of insoluble, Pb210-enriched particles 
deposited at bifurcations and by the ingrowth of Po210 in these particles.
(7,8) Radford and Martell (9) confirmed that the excess Po210 in the
bronchial epithelium of smokers is accomplished by a larger excess of Pb210.
  Fleischer and Parungo (10) provided experimental evidence indicating that
radon decay products and Pb210 are concentrated on trichome tips.  Mechanisms
of accumulation of Pb210 on tobacco trichomes are discussed by Martell and 
Poet. (11)
  Two recent studies (12,13) indicate that alpha radiation from inhaled
indoor radon progeny may explain the incidence of lung cancer in nonsmokers.
Martell and Sweder (14) report that indoor radon decay products that pass
from the room air through burning cigarettes into mainstream smoke are 
present in large, insoluble smoke particles that are selectively deposited
at bifurcations.  Thus, the smoker receives alpha radiation at bronchial
bifurcations from these three sources: from indoor radon progeny inhaled
between cigarettes, from Po214 in mainstream smoke particles, and from
Po210 that grows into Pb210 enriched particles that persist at bifurcations.

|to aviod confusion, when they say Po210 grows into Pb210 enriched
|particles, they mean that the Pb210 breaks down leaving Po210 deposits
|in its place.

I estimate that the cumulative alpha dose at the bifurcations of smokers
who die of lung cancer is about 80rad (1600rem) -- a dose sufficient to induce
malignant transformations by alpha interactions with basal cells.

|This is the clincher here, for me.  If Martell's estimate of the dosage
|at bifurcations is anywhere near accurate, then Po210 must account for
|a large portion of the lung cancer risk from tobacco.

Edward A Martell, Ph.D.
National Center for Atmospheric Research
Boulder, CO 80307

1. Winters TH, DiFranza JR.  Radioactivity in Cigarette Smoke.  NEJM 1982
2. Radford EP, Hunt VR. Polonium-210: a volatile radioelement in cigarettes.
   Science. 1964; 143:247-249
3. Little JB, Radford EP, McCombs HL, Hunt VR. Distribution of polonium-210
   in pulminary tissues of cigarette smokers.  NEJM. 1965; 273:1343-1351
4. Holtzman RB, Ilcewicz FH.  Lead-210 and polonium-210 in tissues of
   cigarette smokers.  Science. 1966; 153:1259-1260
5. Little JB, Radford EP.  Polonium-210 in bronchial epithelium of cigarette
   smokers.  Science. 1967; 155:606
6. Holtzman RB. Polonium-210 in bronchial epithelium of cigarette smokers.
   Science.  1967; 155:607
7. Martell EA.  Radioactivity in tobacco trichomes and insoluble cigarette
   smoke particles.  Nature. 1974; 249:215-7
8. Martell EA.  Tobacco radioactivity and cancer in smokers.  Am Sci. 1975;
9. Radford EP, Martell EA.  Polonium-210: lead-210 ratios as an index of
   residence times of insoluble particles from cigarette smoke in bronchial
   epithelium.  In: Walton WH, ed.  Inhaled particles, part 2.  Oxford:
   Pergamon Press, 1977:567-580
10.Fleischer RL, Parungo FP.  Aerosol particles on tobacco trichomes. 
   Nature. 1974; 250:158-159
11.Martell EA, Poet SE.  Radon Progeny on Biological Surfaces and their
   effects.  In: Vohra KG, et al., eds.  Proceedings, Bombay Symposium on
   Natural Radiation in the Environment.  New Delhi:  Wiley Eastern Ltd., 1982
12.Evans RD, Harley JH, Jacobi W, Mclean AS, Mills WA, Stewart CG.
   Estimate risk from environmental exposure to radon-222 and its decay 
   products. Nature. 1981;290;98-100
13.Harley NH, Pasternack BS. A model for predicting lung cancer risks induced
   by environmental levels of radon daughters.  Health Phys. 1981; 40:307-16.
14.Martell EA, Sweder KS.  The roles of polonium isotopes in the etiology
   of lung cancer in cigarette smokers and uranium miners.  In: Gomez M, ed.
   Proceedings of a symposium on radiation hazards in mining.  New York:
   American Institute of Mining Engineers, 1982:383-389.


  To the Editor:  The presence of Po210 and Pb210 in cigarette smoke may
help to explain a paradox found in smokers of low-tar, low-nicotine
  Hammond et al. (1) noted that the number of deaths from lung cancer was
greater in subjects who smoked 20 to 39 low-tar, low-nicotine cigarettes
a day than in those who smoked one to 19 high-tar, high-nicotine
cigarettes a day.  Thus, the number of cigarettes smoked may be more 
important than their tar and nicotine content.
  Two features of low-tar low-nicotine cigarettes that help to reduce
the amounts of tar in inhaled smoke may have little effect or adverse
effects on the amounts of Po210 and Pb210 in inhaled smoke.  In the
first place, the use of higher porosity paper and perforated filters may
enhance the completeness of combustion.  Although this may decrease the
tar and nicotine content in inhaled smoke, it may increase the pyrolysis
of trichomes, resulting in smoke particles with higher specific activities
of Pb210.  Secondly, cigarette filters have been shown to have no 
noticeable protective effect against Po210 inhalation. (2)  If Po210
and Pb210 contribute to tobacco related cancer, then the number of 
cigarettes smoked may be more important than the tar or nicotine content.
  Although intensive effort has been successful in producing low-tar,
low-nicotine cigarettes, perhaps future research should be aimed toward
the development of low Po210, low Pb210 cigarettes.

Jeffrey I. Cohen M.D.
Duke University Medical Center
Durham, NC 27710

1. Hammond EC, Garfinkel L, Seidman H, Lew EA. Some Recent findings concerning
   cigarette smoking.  In: Origins of Human Cancer.  New York:  Cold Spring
   Harbor Laboratory, 1977:101-112
2. Rajewski B, Stahlholfen W. Polonium-210 activity in the lungs of cigarette
   smokers.  Nature. 1966; 209:1312-1313


  To the Editor:  Contrary to the contention of Winters and DiFranza that
research into the carcinogenic potential of the radioactive component of
cigarette smoke is conspicuous by its absence, we and others have studied
and reported on this risk since the theory was first proposed by Radford
and Hunt in 1964. (1)  Within five years of the initial report that the
radioactive alpha emitter Po210 was present in mainstream smoke and in samples
of bronchial epithelium from cigarette smokers, results from over two dozen
related studies were published.  The source of the Po210 and Pb210 (The
beta emitter Pb210 is the long lived precursor that supports the Po210) was
investigated, (2) the contents of these nuclides in various tobaccos
documented, (3) the fraction transferred to the mainstream or sidestream
smoke (or both) determined, (4) and the concentration in the whole lungs
of smokers and nonsmokers measured. (5)
  Measurements made with cigarette smoke condensate demonstrate that although
radium and thorium are also present in cigarette smoke, 99% of the alpha
activity is from Po210. (6)  Measurements of the whole lungs of smokers and
exsmokers show that the inhaled Po210 is retained in the lower lung. (7)
  A relatively new detection technique using nuclear-track-etch film has
allowed us to determine the amount and microdistribution of alpha activity
on the bronchial mucosa in fresh autopsy specemins. (8)  We examined about
one-fourth of the upper respiratory tract in each of seven persons (Three
smokers, two exsmokers, and two nonsmokers).  A few areas of slightly
elevated alpha activity were found in each of the bronchial trees examined
except that of one young smoker, in which efficient bronchial clearance would
be expected.  The average dose rate to the basal cells of the bronchial 
epithelium from alpha activity in these seven persons ranged from 2.0 to
40mrem per year.  For comparison, the natural background dose from inhaled
radon-daughter alpha activity is about 2000mrem per year.  One area of
a few square millimeters, containing markedly elevated activity, was found
in the bronchii of an older smoker.  This area could deliver an annual dose
of about 20,000mrem, comparable to the results originally reported by
Bradford and Hunt.  This activity can lead to a lifetime dose similar to
the alpha dose that appears to yield an elevated risk of lung cancer in
underground miners.  However, the total dose cannot be calculated, since the
residence time of such an alpha emitting spot on the bronchial tree is not 
  The importance of proper assessment of the risk to cigarette smokers
from radionuclides in the smoke cannot be overstated.  In veiw of the present
knowledge, it is improbable that a single area of a few square millimeters
of high alpha activity in the bronchial tree is important.  Nonetheless,
Po210 is the only component in cigarette smoke tar that has produced cancers
by itself in laboratory animals as a result of inhalation exposure. (9)

|I would question the way they casually play off the signifigance of
|the hot spot here.  Also, I find it rather unusual that locating
|and isolating a single component of tobacco smoke which does produce
|lung cancer by inhalation did not result in a huge investigation of Po210.
|Or at least better media coverage.

  We firmly believe that the role of alpha radiation in tobacco related 
carcinogenesis deserves further study.  The techniques to define its role
in this disease are now available.

Beverly S. Cohen, Ph.D.
Naomi H. Harley, Ph.D.
New York University School of Medicine

New York, NY 10016

1. Radford EP, Hunt R. Polonium-210: a volatile radioelement in cigarettes.
   Science. 1964; 143:247-249
2. Tso TC, Harley NH, Alexander LT.  Source of Pb210 and Po210 in tobacco.
   Science. 1966; 153:880-882
3. Black SC, Bretthauer EW.  Polonium in tobacco.  Radiat Health Data Rep.
4. Ferri ES, Christiansen H.  Lead-210 in tobacco and cigarette smoke.
   Public Health Rep. 1967; 82:828
5. Hill CR.  Polonium-210 in man.  Nature 1965; 208:423-428
6. Cohen BS, Eisenbud M, Harley NH.  Alpha radioactivity in cigarette smoke.
   Radiat Res. 1979;83:190-196
7. Cohen BS, Eisenbud M, Wrenn ME, Harley NH.  Distribution of polonium-210
   in the human lung.  Radiat Res. 1979;79:162-168
8. Cohen BS, Eisenbud M, Harley NH.  Measurement of the alpha activity on
   the mucosal surface of the human bronchial tree. Health Phys. 1980:619-632.
9. Yuille CL, Berke HL, Hull T.  Lung cancer following Pb210 inhalation in 
   rats.  Radiat Res. 1967;31:760-774


  To the Editor:  The letter of Winters and DiFranza has renewed the earlier
suggestion that the radioisotope Po210 may have an important role in the 
induction of lung cancer in smokers.  In particular, it is claimed that
the radionuclide may be deposited very inhomogeneously in the bronchial
epithelium, in the form of a limited number of relatively "hot'' particles,
and that such hot particles may be much more effective carcinogenically
than the same amount of radioactivity would be if it were more uniformly
distributed.  The basis of both these claims must be questioned.
  Evidence on the question of the carcinogenicity of hot particles has
been reviewed by the International Commission on Radiological Protection, (1)
which found the actual situation to be just the reverse of that suggested
by the correspondents.  The evidence cited for the actual formation of
hot particles (2) comes from a study of the Po210 in a series of several
very small samples of bronchial epithelium (usually less than 25 mg)
collected from smokers' lungs.  In these measurements, the activities in 
individual samples were so low that for a proportion at least, only about
20 counts were recorded in a counting period of three to seven days against
a background of 40 counts.  Proper analysis of the statistical validity
of these observations was not given by the original authors and is not
possible from their reported data.  Contrary evidence, not cited by the
correspondents, is provided by a somewhat earlier paper (3) that reported
the results of auto radiographic examination of excised segments of 
bronchial epithelium; this study found no evidence of surface concentrations
of alpha activity of more than 0.01pCi per square centimeter, corresponding
to a mean dose rate of about 10mrem per year.  Finally, the correspondents'
suggestion that the "major source of the polonium is phosphate fertilizer''
is not substantiated and is at variance with published data (3,4) indicating
that it originates as atmospheric fallout of the decay products of natural

|This guy sounds like he knows what he's talking about, see the
|rebuttal in the last letter before you make up your mind, though

C.R. Hill, M.D.
Institute of Cancer Research
Royal Marsden Hospital
Sutton, Surrey SM2 5PX,

1. International Commission on Radiological Protection.  Biological effects
   of inhaled radionuclides, ICRP Publication 31, Section G, 86-92.  Ann ICRP.
   1980;4 (No. 1/2)
2. Little JB, Radford EP, McCombs HL, Hunt VR.  Distribution of polonium-210
   in pulminary tissues of cigarette smokers.  NEJM 1965;273:1343-1351
3. Hill CR.  Polonium-210 in man.  Nature. 1965; 208:423-428
4. Hill CR.  Lead-210 and polonium-210 in grass.  Nature, 1960; 187:211-212


  To the Editor:  The Surgeon General's recent denunciation of tobacco
smoking and the American Cancer Society's pessimistic prognosis that
lung cancer will be the number one cause of death from cancer in women
by 1985 (1) provide timely emphasis on the recent NEJM letter on radioactive

|anyone know if this came true, or is breast cancer still in the lead?
|Just wondering...

alpha emitters in tobacco smoke.  Some of the further study encouraged by
Winters and DiFranza has in fact been performed, yielding results far more
foreboding than expected.
  In two separate studies, Little et al. (2,3) have induced respiratory
tumors in hamsters by intratracheal instillation of Po210 in various
amounts down to less than one-fifth that inhaled by a heavy cigarette
smoker (one who consumes two packs a day) during 25 years.  The incidence
of tumors at the lowest dose was 13%, including borderline carcinomas, and
was 11% for frankly malignant tumors.
  Contrary to the expected results of most radiobiologists, dose reduction
did not result in either a constant dose-response ratio (the linear response
hypothesis) or a larger dose-response ratio (The threshold or sigmoid
hypothesis) but instead produced a marked decrease in the dose-response
ratio.  In one study, a reduction in activity from 0.700microCi of Po210
instilled to 0.00375microCi of Po210 instilled -- about a two hundred-fold
decrease -- resulted in a decrease in the incidence of tumors from 61% to
13% (including borderline cases) -- only a fourfold decrease.

|So this means, as this guy will get to, that doubling your radiation
|exposure at low levels (like the one you are experiencing right now)
|more than doubles your cancer risk.
|Of course, it does have to become asymptotic at 100%, but I, for
|one, do not care to get that far...

  This decrease in the dose-response ratio with decreasing dose has also
been observed in other studies of the effects of low dose alpha radiation
and other radiation particles with high linear energy transfer (LET).  In
a study of osteosarcoma induction by alpha radiation,  Muller et al. (4)
had over a 100-fold decrease in the dose-response ratio from their highest
dose (1500rad) to their lowest dose (15rad).  For neutron radiation, Rossi
et al. (5) found similar results, with leukemia induction having the smallest
dose-response ratio in the lowest dose in survivors of the atomic bomb.
Similarly, Hall et al. (6) found that both dose protraction and dose 
reduction for neutron radiation increased the cell-lethality-dose ratio
of hamster cells in vitro.
  The importance of these results with low dose irradiation by high LET
particles should not be overlooked.  Doses in the range of several thousand
to 10^5 rad have generally been necessary for the experimental induction
of lung cancer by beta or gamma radiation (with low LET), (7,8)  as compared
with the studies by Little et al., in which the lowest dose of 15rad 
(0.00375microCi in the lung volume for the lifetime of the hamsters) induced
cancer at an incidence of about 13%.
  Presumably, the high density of ionization along the track of alpha 
radiation (about one ion pair for every 2 Angstrom traveled) and other
high-LET radiation is the prime factor causing Po210 to be an extremely
efficient carcinogen.
  Clearly, further work is warranted in this area, but we should not hesitate
to disseminate the information already at hand -- that the alpha-radiation
exposure to the lungs of tobacco smokers is extremely important.

Walter L. Wagner, B.A.
Veterans Administration
Medical Center
San Francisco, CA 94121

1. American Cancer Society. Ca: a cancer journal for clinicians. Jan/Feb
   1981;Vol 31, No. 1
2. Little JB, Kennedy AR, McGandy RB. Lung cancer induced in hamsters by
   low doses of alpha radiation from polonium-210.  Science. 1975; 188:737-738
3. Little JB, O'Toole WF.  Respiratory tract tumors in hamsters induced by
   benz(a)pyrene and Po210 radiation.  Cancer Res. 1974; 34:3026-3039
4. Muller WA, Gossner W, Hug O, Luz A.  Late effects after incorporation of
   the short-lived alpha-emitters Ra224 and Th227 in mice.  Health Phys. 1978;
5. Rossi HH, Mays CW. Leukemia risk from neutrons.  Health Phys. 1978; 
6. Hall EJ, Rossi HH, Roizin LA.  Low-dose-rate irradiation of mammalian cells
   with radium and californium-252.  Radiology. 1971; 99:445-451
7. Cember H.  Radiogenic Lung Cancer.  Prog Exp Tumor Res. 1964; 4:251.
8. Sanders CL, Thompson RC, Blair WJ. AEC Symp Ser. 1970; 18:285.


  To the editor: The letter by Winters and DiFranza rivets much needed 
attention on the earlier finding of Radford and Hunt, (1) which is crucial
to an understanding of the pathogenesis of smoking diseases. (2,3)
  Although Winters and DiFranza tellingly describe the mechanisms by which 
Po210 on insoluble particles in cigarette smoke causes lung cancer, they
neglect the even more important matter of how Po210 and other mutagens
from tobacco smoke cause malignant neoplasms, degenerative cardiovascular
diseases, and other diseases throughout the body of smokers (Table 1).

|Though he may be right, I have to moan at the way this guy just took
|this data and slapped a new header on it.  It's not even descriptive!
|What exactly do the numbers in the feilds mean? Ugh.

TABLE 1. Effects of Smoking on Tissues Directly and Indirectly Exposed
         to Radiation in Current Cigarette Smokers*
         Cause of Death                Number of Deaths     Observed/


         All causes                    36,143   20,857        1.73
         Emphysema                      1,201       81       14.83

         Of directly exposed tissue     3,061      296       10.34
           Of buccal cavity               110       26        4.23
           Of pharynx                      92        7       13.14
           Of larynx                       94        8       11.75
           Of lung and bronchus         2,609      231       11.29
           Of esophagus                   156       24        6.50

         Of indirectly exposed tissue   4,547    3,292        1.38
           Of stomach                     390      257        1.52
           Of intestines                  662      597        1.11
           Of rectum                      239      215        1.11
           Of liver and biliary passages  176       75        2.35
           Of pancreas                    459      256        1.79
           Of prostate                    660      504        1.31
           Of kidney                      175      124        1.41
           Of bladder                     326      151        2.16
           Of brain                       160      152        1.05
           Malignant lymphomas            370      347        1.07
           Leukemias                      333      207        1.61
           All other cancers              597      407        1.47

         All cardiovascular diseases   21,413   13,572        1.58
           Coronary heart disease      13,845    8,787        1.58
           Aortic aneurysm                900      172        5.23
           Cor pulmonale                   44        8        5.50
           All other cardiovascular     6,624    4,605        1.44

         Ulcer of stomach, duodenum
           or jejunum                     289       93        3.10

         Cirrhosis of liver               404      150        2.69
         *Data adapted from Rogot and Murray. (4)

|At any rate: here I put forth the question -- if some of these
|ailments are generated at ten times+ the rate in smokers as in
|non smokers, as this table indicates, supposing marijuana is
|carcinogenic in the same manner as tobacco, wouldn't it be relatively
|easy, even in this country, to find a correlation??  I submit
|this as a second proof that the chemical tar component has little to do
|with the majority of lung cancer deaths

  Volatilized, soluble Po210, produced at the burning temperature of
cigarettes, (1) is cleared from the bronchial mucosa at the expense of
the rest of the body, being absorbed through the pulmonary circulation
and carried by the systemic circulation to every tissue and cell, causing
mutations of cellular genetic structures, deviation of cellular 
characteristics from their optimal normal state, accelerated aging, and
early death from a body-wide spectrum of diseases, reminiscent of the
disease and mortality patterns afflicting early radiologists and others
with long-term exposure to x-rays and other forms of ionizing radiation. (5,6)
  The proof of circulating mutagens from smoking is that Po210 and other
mutagens can be recovered not only from tobacco smoke and bronchial mucosa,
but also from the blood and urine of smokers. (1,7)

R.T. Ravenholt M.D., M.P.H.
Centers For Disease Control
Washington Office
Rockville, MD 20857

1. Radford EP Jr, Hunt VR.  Polonium-210: a volatile radioelement in
   cigarettes.  Science. 1964; 143:247-249
2. Ravenholt RT. Malignant cellular evolution: an analysis of the causation
   and prevention of cancer.  Lancet. 1966; 1:523-526
3. Ravenholt RT, Lavinski MJ, Nellist D, Takenaga M.  Effects of smoking
   upon reproduction.  Am J Obstet Gynecol. 1966; 96:267-281
4. Rogot E., Murray JL.  Smoking and causes of death among U.S. veterans:
   16 years of observation.  Public Health Rep. 1980:213-222
5. Warren S.  Longevity and causes of death from irradiation in physicians.
   JAMA. 1956; 162:464-468
6. National Academy of Sciences-National Research Council.  Long term effects
   of ionizing radiation from external sources.  Washington D.C.:  National
   Research Council, 1961.
7. Office on Smoking and Health.  Smoking and Health: a report of the 
   Surgeon General.  Rockville, MD: Office on smoking and health, 1979.
   (DHEW publication no. [PHS]79-50066).


  To the editor:  We concur with Drs. Winters and DiFranza that the scientific
and medical community as well as public health officials should be more 
concerned with the detrimental effects of cigarette smoking.  Reviews on the 
carcinogenic effect of cigarette smoke are made available to United States
physicians at regular intervals through the Surgeon General's reports
entitled Smoking and Health. (1)  From these reports it is clear that
benzo(a)pyrene is by far not the only carcinogen identified in cigarette
smoke.  Benzo(a)pyrene serves merely as an indicator for the wide 
spectrum of carcinogenic polycyclic hydrocarbons, all of which are 
pyro synthesized by the same mechanism during smoking.  Aside from these
hydrocarbons, cigarette smoke contains other carcinogens such as aza-arenes,
aromatic amines (including beta-napthylamine), nickel, volatile nitrosamines,
and especially tobacco-specific N-nitrosamines. (1-3)  The N-nitrsamine
compounds are formed by nitrosation of nicotine and other alkaloids; their 
concentrations in tobacco and smoke exceed those of nitrosamines found in
other consumer products by at least several hundred fold.  These nitrosamines
are probably formed from nicotine in vivo. (2,3)  Above all, one needs to
consider that the carcinogenic potential of tobacco is a composite effect
of tumor initiators, tumor promoters, or co-carcinogens, and organ-specific
carcinogens. (1,2)

Dietrich Hoffmann, Ph.D.
Ernst L. Wynder, M.D.
American Health Foundation
New York, NY 10017

1. Office on smoking and health.  Smoking and Health: a report of the
   Surgeon General.  Rockville, MD: Office on smoking and health, 1979.
   (DHEW Publication No. [PHS]79-50066)
2. Wynder EL, Hoffman D.  Tobacco and health: a societal challenge.
   NEJM 1979; 300:894-903
3. Hofmann D, Adams JD, Brunnemann KD, Hecht DD.  Formation, occurrence
   and carcinogenesity of N-nitrosamines in tobacco products.  Am. Chem.
   Soc. Symp. Ser. 1981; 174:247-273


  To the editor: We thank Dr. Martell and Drs. Cohen and Harley for their
reviews of the literature.  Judging by the response to our original letter,
research into the radioactive component has been in progress since the
early 1960's, but the existence of this research is largely unknown outside
a small segment of the scientific community.  We were gratified to receive
hundreds of phone calls from smokers who quit on learning about the alpha
radiation in cigarette smoke.
  Hill examined the lungs of only two smokers old enough to have metaplastic
lesions.  In addition, he analyzed whole bronchial specemins weighing 5g to
15g, of which only 2% by weight was epithelium.  His result of 0.007 pCi
per gram of tissue is in reasonable agreement with Little's result of 0.012pCi 
per gram of whole bronchus and thus does not disprove the existence of hot
spots.  In addition, the accumulation of Pb210 on tobacco leaves is from
natural and unnatural radon-222 decay products and from phosphate fertilizers.

| I really wish they had cited the source for this last part, as it
|hasn't been documented to my total satisfaction
|All I have is a chart of the concentration of Po210 and Pb210 in
|various tobacco from different parts of the world.  It shows India
|as the lowest.  The US fertilizes with phosphates rich in Radium and
|other radioisotopes.  It was second highest.  I don't know what the
|Soviet Union is up to as far as fertilizer, but it got the dubious
|distinction of first place.  Maybe they farm their tobacco near
|Chebalinsk (sp?)  (site of cover up of nuclear disaster bigger than
|Chernobal) |-\ Of course by now anywhere in the Soviet Union is New Jersey.
|[gonna have to look up the name of that place again, where's my
|Mother Jones??]

  We thank Dr. Wagner for pointing out that alpha radiation now appears to
be 1000 times more carcinogenic than gamma radiation.  Standard practice
reguards alpha radiation as only 10 to 20 times as carcinogenic as gamma

|Sing along now:
|That's a good thing to know!
|That's a very good thing to know!
|Makes me want to jump and sing!
|I'm so glad I know that thing!

  The growing list of malignant diseases associated with smoking, presented
by Dr. Ravenholt, begs for causal explanation.  Smokers have higher levels 
of Po210 in the lungs, bone blood and urine. (1-3)  Higher levels of Po210
have been consistently found in smokers in the liver, kidney, spleen,
pancreas, and gonads. (4,5)  A study with an adequate number of subjects
would probably demonstrate a significant difference.  The Po210 must be
strongly considered as a cause of these cancers.
  Drs. Cohen and Harley report finding one "hot spot'' on studying the
alpha activity of alpha Po210 in tracheal autopsy specemins of seven people,
three of whom were smokers. (6)  This supports Little and his colleagues' 
previous findings of "hot spots'' in 7 out of 37 smokers.
  We thank Drs. Hoffmann and Wynder for correcting us about the variety
of chemical carcinogens present in cigarette smoke.  It is possible that
chemicals and Po210 act as cocarcinogens in the following manner.  Chemical
and possibly physical agents create metaplastic nonciliated epithilial
lesions.  Auerbach demonstrated such lesions in 100% of heavy smokers. (7)
The Po210 present on insoluble particles gains entrance to epithelial cells
in such non-ciliated areas of mucous stagnation.  Ingrowth of Po210 from the
decay of Pb210 results in high doses of alpha radiation to already metaplastic
cells. (8)  Continued smoking ensures a steady delivery of Pb210 to these
stagnant sites.  Little and his co-workers have demonstrated synergism 
between benzo(a)pyrene and Po210 in an animal model. (9)
  In view of the potential role of alpha radiation in a variety of tobacco
related neoplasias, we believe that this area deserves more intense research.
We find it surprising that the National Cancer Institute, with an annual
budget of $500 million, has no active grants on alpha radiation as a cause
of lung cancer (National Cancer Institute: personal communication).
  We have found when educating smokers that more are encouraged to quit
as they learn of the presence of radiation in cigarette smoke.

|Ahh.  My point.  Glad I'm not the only owner.

Joseph R. DiFranza, M.D.
Thomas H. Winters, M.D.
University of Massachusetts Medical Center
Worcester, MA 01605

1.  Little JB, Radford EP Jr, McCombs HL, Hunt VR.  Distribution of 
    polonium-210 in pulminary tissues of cigarette smokers. NEJM 1965;
2.  Radford EP Jr, Hunt VR.  Polonium-210: a volatile radioelement in
    cigarettes.  Science. 1964; 143:247-249
3.  Holtzman RB, Ilcewicz FH.  Lead 210 and Po210 in tissues of cigarette
    smokers. Science. 1966; 153:1259-1260
4.  Blanchard RL.  Concentrations of Pb210 and Po210 in human soft tissues.
    Health Phys. 1967; 13:625-632.
5.  Hill CR.  Polonium 210 in man.  Nature. 1965; 208:423-428
6.  Cohen BS, Eisenbud M, Harley NH.  Measurement of the alpha radioactivity
    on the mucosal surface of the human bronchial tree.  Health Phys. 1980;
7.  Auerbach O, Stout AP, Hammond EC, Garfinkel L.  Changes in bronchial
    epithelium in relation to cigarette smoking and in relation to lung
    cancer.  NEJM 1961; 265:253-67
8.  Radford EP, Martell EA.  Polonium 210/Lead 210 ratios as an index of
    residence times of insoluble particles from cigarette smoke in bronchial
    epithelium.  In: Walton WH, ed. Inhaled Particles. IV. Part 2, Oxford,
    Pergamon Press, 1977:567-580
9.  Little JB, McGrandy RB, Kennedy AR.  Interactions between polonium 210
    alpha radiation, benzo(a)pyrene, and 0.9% NaCl instillations in the
    induction of experimental lung cancer.  Cancer Res. 1978; 38:1929-1935. 


|Also, a thank you to the origional poster of this article, whose
|name I have unfortunately lost in one of those funky little
|crevasses that you can't help but find every time you learn a new
|text editor.

		6 on EPA Panel Tied to Tobacco Group
	  Chicago Tribune, Friday, November 9, 1990, page 3.

"NEW YORK (AP) Six of the 16 members of a newly appointed
Environmental Protection Agency panel considering the health risks of
second-hand cigarette smoke have ties to a tobacco industry research
organizations, documents show.

A seventh member of the panel was appointed on the recommendation of
the Philip Morris tobacco company, EPA officials said.

"They've stacked the deck with people who have closed ties to the
tobacco industry,"said Dr. Alan Blum, a founder of the anti-smoking
group, Doctors Ought to Care. "It's pathetic"

"We were concerned about the appearance of conflict of interest," said
Donald Barnes, staff director of the EPA's scientific advisory board.
But he said the link between the panel members and the tobacco
organization "does not  cause any question to be raised [sic] about
their technical capabilities."

The panel is to review the scientific accuracy and objectivity [sic]
two forthcoming EPA reports on the health effects of passive smoking.

Six members are connected with the Center for Indoor Air Research of
Linthicum, Md., according to the centers' publications. 

The center is financed by Philip Morris, R.J Reynolds Tobacco Co. and
Lorillard Corp., three of the nation's largest tobacco companies. Its
board of directors are made up of employees of those companies, said a
center administrator.

The chairman of the EPA passive-smoking panel, Morton Lippmann of New
York University, is on the science advisory board of the tobacco
industry center. Lippmann and another member of the EPA panel, Dr.
Jonathan Samet of the University of New Mexico, helped devise the
center's research agenda. Samet and three other members of the EPA
panel are listed as "peer reviewers" for the center.

Yet another member, of the EPA panel, Delbert Eatough of Brigham Young
University, received research funds from the center.

A seventh member of the panel, Geoffrey Kabat of the American Health
Foundation, had been recommended [sic]  by Philip Morris, EPA
officials said.


The makeup of the EPA panel aroused controversy when it was reported
last month that the agency had dismissed Dr. David Burns from the
panel after the tobacco industry lobbied to get rid of him.

Burns,  of the University of California at San Diego, was the author
of the U.S. Surgeon General's report on passive smoking and is
regarded by his colleagues as a leading authority on passive smoking.
He was reinstates to the EPA panel after his dismissal was disclosed.

Lippmann said he didn't see any problems working with the EPA  and with
the tobacco research center.


Lippmann said three of his colleagues at New York University's
Institute of Environmental Medicine, where Lippmann works,  have
received grants from the tobacco industry group. The largest grant was
for $250,000 [sic], he said.

Eatough, who has received research funds from R.J. Reynolds as well as
the Center for Indoor Air Research [above-mentioned tobacco-industry
corporations "center"] , said the receipt of such money does not
compromise his objectivity.



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