The information provided on this website
is for informational and educational purposes only. It is not intended
as a substitute for professional health care. The author of this overview
(and the creator of this website), is a very experienced acinic cell carcinoma
patient and well-informed layperson, but not a physician. Statements here
are offered as opinions, not as licensed or professional medical advice.
The reader is advised to consult with health professionals regarding medical
diagnoses or treatments.
No one knows definitively what causes Acinic Cell Carcinoma. Just as with
the rest of this disease, little or no research has been done in this
area. And in general, the definitive causes for most cancers are unknow
n. It is also likely that there is no SINGLE cause for Acinic Cell Carcinoma.
Probably it has to do with multiple factors, including environmental and
genetic. And the causes likely vary from individual to individual. So
if you are looking for something to “blame” the cancer on, you
will probably not find the ultimate answer here. HOWEVER, there is a little
bit of evidence and research to point you in some theoretical directions.
We have included as much as we have found.
One potential cause that has been attributed for this disease is previous
radiation exposure, specifically radiation for thyroid disease. Environmental
radiation (from nuclear bombs, testing, accidents) has been shown to be
a cause of other salivary gland cancers, if not acinic cell specifically.
However, there have been anecdotal cases of acinic cell patients or their
doctors attributing their cancer to nuclear and atomic bomb testing. Ionizing
radiation in general has been implicated as a cause for other salivary
gland cancers.
Other possible causes that have been cited in the literature are: 1) a
familial predisposition in parotid cancer, 2) chronic wood dust inhalation
in certain individuals who develop minor salivary gland adenocarcinomas
of the nasal and paranasal sinuses. Another theoretical cause has been
attributed to radiation from Tungsten/Halogen light sources. This has
been shown to cause various forms of skin cancer. It has not been studied
in relation to salivary gland cancers, but there is some anecdotal experience
to raise suspicions that this may be a factor here as well. Another possible
carcinogen related cause is second-hand smoke. Both of the last two potential
causes are theoretical and anecdotal only. They have been implicated in
other cancers, but not ACC specifically.
If any of you out there have experiences to strongly indicate a cause
for YOUR case (or your patient’s) please let us know.
It is worth noting that certain carcinogenic agents have been used to
induce Acinic Cell Carcinoma tumors in animal studies. ACC has been
induced in rats with the agent Azaserine. Also of note is that in
routine pharmaceutical testing, carcinogenesis is sometimes discovered.
We know of at least one drug; Neurontin (Gabapentin) that has induced
ACC tumorigenesis in rats. Specifically, a statistically significant
increase in the incidence of pancreatic acinar cell adenomas and carcinomas
was found in male rats receiving high doses of this medication.
We have included any possibly relevant literature and links below. Some
of the literature does not mention ACC, and is only theoretical in its’
inclusion here. We have also created a table of any literature specifically
mentioning Acinic Cell Carcinoma and possible causes.
(Note: Both these buttons are inactive at this time.)
Partial Bibliography (more to be added
later):
Cancer: Principles & Practice of Oncology, 6th Editions
Author(s): Vincent T. DeVita, Jr., MD, Samuel Hellman, MD, Steven A. Rosenberg,
MD, PhD
Date: January 2001
Chapter 30.4: Tumors of the Salivary Glands and Paragangliomas
Roy B. Sessions, Louis B. Harrison, Arlene A. Forastiere
Major Salivary Gland Tumors
Katz A, Preston-Martin S. Salivary gland tumors and previous radiation
therapy to the head and neck. Am J Surg 1984;147:345.
Hollander L, Cunningham M. Management of cancer of the parotid gland.
Surg Clin North Am 1973;53:113.
Klintenber C, Olofsson J, Hellquist H, Sokjer H. Adenocarcinoma of the
ethmoid sinuses: a review of 28 cases with special reference to dust exposure.
Cancer 1984;54:482.
Textbook of Uncommon Cancer, 2nd Ed., pp 408.
Section on Acinic Cell Carcinoma
ACC CAUSE – RELATED ARTICLES, BOOK EXCERPTS
& LINKS
Salivary Gland Cancer (PDQ®): Treatment
- General Information
Natl. Cancer Institute website: cancer.gov
PDQ on Salivary Gland Cancers:
Health Professional Version
http://www.cancer.gov/cancer_information/doc_pdq.aspx?viewid=435800F6-1D0B-41BA-B2A5-678745E14C3F&version=1#3
Date Last Modified: 8/2002
Excerpt: There is a definite association between radiation to the
head and neck area and the development of salivary gland tumors.
The influence of chronic pancreatitis on
carcinogenesis: an experimental study in rats.
Bednarz W, Olewinski R.
First Department of General and Endocrine Surgery, Medical Academy, Wroclaw,
Poland.
Eur J Gastroenterol Hepatol 2002 Jun;14(6):671-7
Courtesy PubMed/NCBI
The risk
of development of carcinoma of the exocrine part of the pancreas in patients
with chronic pancreatitis is studied. Researchers performed an experimental
study to define the risk of carcinogenesis in the course of chronic pancreatitis
in rats. Results demonstrated that chronic pancreatitis in rats predisposes
to malignant proliferative lesions, including acinic cell carcinoma.
Expression of the protein product of p53 gene mutations correlated with
neoplastic transformation of pancreas preceded by chronic pancreatitis.
The influence of chronic pancreatitis on
carcinogenesis: an experimental study in rats.
Bednarz W, Olewinski R.
First Department of General and Endocrine Surgery, Medical Academy, Wroclaw,
Poland.
Eur J Gastroenterol Hepatol 2002 Jun;14(6):671-7
BACKGROUND: The literature contains many controversial or unclearly defined
opinions about the risk of development of carcinoma of the exocrine part
of the pancreas in patients with chronic pancreatitis. This and our own
clinical observations based on analysis of patients with chronic pancreatitis
treated surgically (anastomotic and resectional procedures) formed the
background to an experimental study to define the risk of carcinogenesis
in the course of chronic pancreatitis in rats. EXPERIMENTAL FINDINGS :
In Wistar rats with chronic pancreatitis induced by etionine and then
exposed to carcinogenic action of azaserine, proliferation, adenomas and
acinic cell carcinomas of the exocrine part of the pancreas were diagnosed;
the carcinomas were transplantable. In rats treated with azaserine only,
benign proliferative lesions and adenomas were found. The presence of
the p53 mutation protein was observed in carcinomatous pancreatic cells
in malignant lesions of the pancreas in primary and transplantable cancers,
but was not detected in benign proliferative lesions and adenomas. Chronic
pancreatitis in Wistar rats predisposes the exocrine part of pancreas
to malignant transformation. Growth of cancers of the exocrine part of
the pancreas in male rats, but not in female rats, suggests hormonal determination
of experimental pancreatic cancer. CONCLUSIONS : Results demonstrate that
chronic pancreatitis in rats predisposes to malignant proliferative lesions,
including acinic cell carcinoma. Expression of the protein product of
p53 gene mutations correlated with neoplastic transformation of pancreas
preceded by chronic pancreatitis, and was also detected in transplantable
tumours.
Brain tumors and salivary gland cancers
among cellular telephone users.
Auvinen A; Hietanen M; Luukkonen R; Koskela RS
Epidemiology 2002 May;13(3):356-9
Finnish Cancer Registry and STUK-Radiation and Nuclear Safety Authority,
Helsinki.
Courtesy PubMed/NCBI
1996 Finnish study of possible cancer
risks of cell phone use. RESULTS: Cellular phone use was not associated
with brain tumors or salivary gland cancers overall, but there was a weak
association between gliomas and analog cellular phones. CONCLUSIONS: A
register-based approach has limited value in risk assessment of cellular
phone use owing to lack of information on exposure.
Brain tumors and salivary gland cancers
among cellular telephone users.
Auvinen A; Hietanen M; Luukkonen R; Koskela RS
Epidemiology 2002 May;13(3):356-9
Finnish Cancer Registry and STUK-Radiation and Nuclear Safety Authority,
Helsinki.
BACKGROUND: Possible risk of cancer associated with use of cellular telephones
has lately been a subject of public debate. METHODS: We conducted a register-based,
case-control study on cellular phone use and cancer. The study subjects
were all cases of brain tumor (N = 398) and salivary gland cancer (N =
34) diagnosed in Finland in 1996, with five controls per case. RESULTS:
Cellular phone use was not associated with brain tumors or salivary gland
cancers overall, but there was a weak association between gliomas and
analog cellular phones. CONCLUSIONS: A register-based approach has limited
value in risk assessment of cellular phone use owing to lack of information
on exposure.
Use of cellular telephones and risk
of cancer. A Danish cohort study
[Article in Danish]
Johansen C, Boice JD Jr, McLaughlin JK, Olsen JH.
Institut for Epidemiologisk Kraeftforskning, Kraeftens Bekaempelse, Strandboulevarden
49, DK-2100 Kobenhavn.
Ugeskr Laeger 2002 Mar 18;164(12):1668-73
Courtesy PubMed/NCBI
The use of cellular telephones has been suggested to increase the risk
of cancer. This Danish study carried out a retrospective cohort study
of the incidence of cancer in 420,095 users of cellular telephones during
the period of 1982 to 1995. Although 3391 cancers were found, this was
less than expected. Authors conclude that the results do not support the
hypothesis of an association between cell phone use and tumours of the
brain or salivary gland, leukemia, or other cancers.
Use of cellular telephones and risk of cancer.
A Danish cohort study
[Article in Danish]
Johansen C, Boice JD Jr, McLaughlin JK, Olsen JH.
Institut for Epidemiologisk Kraeftforskning, Kraeftens Bekaempelse, Strandboulevarden
49, DK-2100 Kobenhavn.
Ugeskr Laeger 2002 Mar 18;164(12):1668-73
INTRODUCTION: The use of cellular telephones has been suggested to increase
the risk of cancer. MATERIAL AND METHODS: We carried out a retrospective
cohort study of the incidence of cancer in all 420,095 users of cellular
telephones during the period of 1982 to 1995. RESULTS: Overall, 3391 cancers
were found, with 3825 expected, which yielded a significantly decreased
standardized incidence ratio of 0.89. No increased incidence was seen
for cancers of the brain or nervous system, of the salivary gland or for
leukaemia, cancers which were of a priori interest. DISCUSSION: The results
do not support the hypothesis of an association between the use of these
telephones and tumours of the brain or salivary gland, leukaemia, or other
cancers.
Salivary Gland Cancer – Detailed Reference Guide
From the American Cancer Society website
http://www.cancer.org/eprise/main/docroot/cri/cri_2_3x?dt=54
As of 2001 (4/16, 8/2 depending on section)
Excerpt of the following sections:
Causes, Risk Factors and Prevention
- What Are The Risk Factors for Salivary Gland Cancer?
- Do We Know What Causes Salivary Gland Cancer?
- Can Salivary Gland Cancer Be Prevented?
Excerpts from a comprehensive overview
of Salivary Gland Cancer, written for patients. Concise and apparently
reliable information on this subject. There may be other cause possibilities
not discussed, but this is a reasonable overview. We also recommend going
to the ACS site directly for updates and revisions, as well as links and
other services they offer.
American Cancer Society
Cancer Reference Information
Detailed Guide:
SALIVARY GLAND CANCER - Causes, Risk Factors and Prevention
What Are The Key Statistics For Salivary
Gland Cancer?
Salivary gland cancers are very uncommon and account for less than 1%
of all cancers, and about 7% of cancers of the head and neck area. The
survival rates for malignant salivary gland tumors depend on the cell
type and the stage of the cancer. The stage of the cancer depends on its
size and whether or not it has spread to other parts of the body. Staging
is discussed in detail in the section "How is Salivary Gland Cancer
Diagnosed?"
What Are The Risk Factors for Salivary Gland
Cancer?
A risk factor is anything that increases a person's chance of getting
a disease such as cancer. Different cancers have different risk factors.
For example, unprotected exposure to strong sunlight is a risk factor
for skin cancer, and smoking is a risk factor for lung, laryngeal, esophageal,
oral, and several other cancers. Scientists have found few risk factors
that make a person more likely to develop salivary gland cancer. Even
if a patient does have one or more risk factors for salivary gland cancer,
it is impossible to know for sure how much that risk factor contributed
to causing the cancer.
Radiation Exposure
If a person has had radiation treatment to the head and neck area for
some other medical reason, the risk of salivary gland cancer increases.
Industrial exposure to certain radioactive substances can also increase
the risk of developing salivary gland cancer.
Other Industrial Exposure
Some studies did not find any relationship between specific occupations
and salivary gland cancer risk. Others suggest that working with certain
metals (nickel alloy dust) or minerals (silica dust) may increase the
risk for salivary gland cancer.
Diet
Some studies have found that a diet that is deficient in vegetables and
high in animal fat increases the risk of developing salivary gland cancer
Tobacco Use
Tobacco use is known to cause squamous cell carcinomas of the mouth and
throat, as well as cancers of several other organs. Tobacco use may also
be a risk factor for squamous cell cancers of the salivary glands, but
it probably does not affect the risk for other types of salivary gland
cancers.
Family History
A high cancer risk may be inherited if many blood relatives of a family
have had cancer. Very rarely, members of some of these families seem to
have a higher than usual risk of developing salivary gland cancers.
Do We Know What Causes Salivary Gland Cancer?
Very little is known about what actually causes the majority of salivary
gland cancers. Researchers have found that some salivary gland cancers
have DNA abnormalities in certain genes. Abnormalities of some genes may
change the way a cell grows or multiplies, or how the cell is recognized
by the immune system. Exposure to radiation or certain carcinogens (cancer-causing
chemicals) may result in these DNA changes but in most cases, their cause
is not known.
Can Salivary Gland Cancer Be Prevented?
Because the cause of most salivary gland cancers is unknown, it is not
possible to recommend ways to prevent them. However, avoiding certain
risk factors may slightly lower the likelihood of developing salivary
gland cancer. For more information, refer to the section "What Are
the Risk Factors for Salivary Gland Cancer?"
People who work with radioactive substances, silica dust, and nickel alloy
dust should take precautions to protect themselves against exposure to
these materials. The American Cancer Society recommends a diet consisting
of a variety of healthful foods, with an emphasis on plant sources. This
should include five or more servings of vegetables and fruits each day,
whole grain foods (such as breads, rice, pasta, and cereal), and limited
intake of red meats, especially those high in fat or processed.
These workplace and dietary precautions may lower a person's risk of developing
salivary gland cancer. Even more importantly, eating a healthy diet and
avoiding exposure to radiation and carcinogens (cancer-causing chemicals)
reduces the risk of developing other, more common cancers.
Cell phone use again cleared of cancer risk
Oncolink Cancer News – Reuters Health Information
http://www.oncolink.upenn.edu/templates/resources/article.cfm?c=3&s=8&ss=23&id=1044
Last Updated: 2001-02-06 16:00:31 EST (Reuters Health)
A nationwide cohort study in Denmark
finds no link between cellular telephone use and tumors of the brain or
salivary gland, leukemia, or other cancers, according to a report published
in the February 7th issue of the Journal of the National Cancer Institute.
Cell phone use again cleared of cancer risk
Oncolink Cancer News – Reuters Health Information
Last Updated: 2001-02-06 16:00:31 EST
A nationwide cohort study in Denmark finds
no link between cellular telephone use and tumors of the brain or salivary
gland, leukemia, or other cancers, according to a report published in
the February 7th issue of the Journal of the National Cancer Institute.
Dr. Christoffer Johansen, from the Danish Cancer Society, in Copenhagen,
and colleagues identified all 420,095 cellular telephone users from subscriber
lists of the two companies that provide service in Denmark, and linked
these data to the Danish Cancer Registry.
While 3825 cancers would be expected in a general population of this size,
only 3391 cancers were observed, the authors state. This decreased risk
was due, in large part, to deficits of lung cancer and other smoking-related
cancers in the study group. In addition, the incidence of brain or salivary
cancers, and leukemia were not increased in cellular telephone users.
The duration of cellular telephone use, time since first subscription,
age at first subscription, or type of telephone had no effect on cancer
risk, the investigators point out. In patients who developed brain and
nervous system tumors, the subtype and anatomic location of the tumor
was not associated with cellular telephone use.
The current findings agree with the results of two recent US studies,
reported by Reuters Health on December 19, 2000, that found that no association
between cellular telephone use and brain cancer. However, a Swedish study
earlier last year did report an increased risk of brain cancer among cellular
telephone users.
In a related editorial, Dr. Robert L. Park, from the American Physical
Society, in Washington, comments that "the public, it seems, is more
easily persuaded by anecdotal accounts than by science, and the scientific
community should bear that in mind when communicating with the public."
"Regardless of how convincing the evidence exonerating cell phones
may be, there will continue to be those who will argue that the issue
has not been completely settled," Dr. Park states.
Reference
* J Natl Cancer Inst 2001;93:166-167,203-207. (Abstract not available
online at time of posting.)
See Also:
* OncoLink: Brain Tumors
* OncoLink: Cancer Genetics
* OncoLink: Childhood Leukemia
* OncoLink: Lung Cancer
* OncoLink: Smoking and Cancer
Excerpt From: Cancer: Principles & Practice
of Oncology, 6th Editions
Vincent T. DeVita, Jr., MD, Samuel Hellman, MD, Steven A. Rosenberg, MD,
PhD
January 2001
Chapter 30.4: Tumors of the Salivary Glands and Paragangliomas
Roy B. Sessions , Louis B. Harrison , Arlene A. Forastiere
Major Salivary Gland Tumors
Considered by many in the worldwide
medical community as the standard-setting oncology reference, Cancer:
Principles and Practice of Oncology is now in its Sixth Edition. This
is an excerpt from the chapter on Major Salivary Gland Tumors, specifically
related to possible causes.
Excerpt From: Cancer: Principles & Practice
of Oncology, 6th Editions
Vincent T. DeVita, Jr., MD, Samuel Hellman, MD, Steven A. Rosenberg, MD,
PhD
January 2001
Chapter 30.4: Tumors of the Salivary Glands and Paragangliomas
Roy B. Sessions, Louis B. Harrison, Arlene A. Forastiere
Major Salivary Gland Tumors;
Etiology, Pathology, and Classification
Excerpt:
The causes of salivary gland cancer have not been determined. Certain
factors have been etiologically suggested, including ionizing radiation
with all salivary cancers,5 a familial predisposition in parotid cancer,6
and chronic wood dust inhalation in certain individuals who develop minor
salivary gland adenocarcinomas of the nasal and paranasal sinuses.7 Proof
of cause and effect does not exist, however, in any of these postulated
associations, and the etiology of most salivary gland cancers cannot be
determined.
5. Katz A, Preston-Martin S. Salivary gland tumors and previous radiation
therapy to the head and neck. Am J Surg 1984;147:345.
6. Hollander L, Cunningham M. Management of cancer of the parotid gland.
Surg Clin North Am 1973;53:113.
7. Klintenber C, Olofsson J, Hellquist H, Sokjer H. Adenocarcinoma of
the ethmoid sinuses: a review of 28 cases with special reference to dust
exposure. Cancer 1984;54:482.
Acinic cell carcinoma: its occurrence in
the laryngotracheal junction after thyroid radiation.
Squires JE, Mills SE, Cooper PH, Innes DJ Jr, McLean WC.
A case of ACC developing in 54 year old woman 46 years after radiation to thyroid gland. Other related data is discussed.
Acinic cell carcinoma: its occurrence in the laryngotracheal junction
after thyroid radiation.
Squires JE, Mills SE, Cooper PH, Innes DJ Jr, McLean WC.
An acinic cell carcinoma of the laryngotracheal junction developed in
a 54-year-old woman 46 years after administration of radiation to her
thyroid gland. Although salivary gland neoplasia has been associated with
a history of radiation therapy during childhood, acinic cell carcinoma
in such a setting is rare. In addition, she had parathyroid hyperplasia
and multiple thyroid adenomas, lesions that have been associated with
prior administration of radiation.
A history of exposure to radiation should be sought in patients with salivary
gland neoplasms of the larynx or trachea.
Familial occurrence of acinic cell carcinoma
of the parotid gland.
Depowski PL, Setzen G, Chui A, Koltai PJ, Dollar J, Ross JS.
Department of Pathology, Albany Medical College, NY 12208, USA.
Arch Pathol Lab Med 1999 Nov;123(11):1118-20
Courtesy PubMed/NCBI
A report of familial occurrence of acinic cell carcinoma (35 year old man and 16 year old daughter). While this may represent a coincidental event, the possibility that this is a result of common genetic or environmental risk cannot be excluded.
Familial occurrence of acinic cell carcinoma
of the parotid gland.
Depowski PL, Setzen G, Chui A, Koltai PJ, Dollar J, Ross JS.
Department of Pathology, Albany Medical College, NY 12208, USA.
Arch Pathol Lab Med 1999 Nov;123(11):1118-20
We report the familial occurrence of acinic cell carcinoma involving
the parotid gland, the first such report of which we are aware. The
familial occurrence of any salivary gland neoplasm is rare. Several reports
are present in the literature, including pleomorphic adenoma, Warthin
tumor, carcinoma of the submandibular gland, and malignant lymphoepithelial
lesion.
We report the case of a 35-year-old man who underwent excision of a left
parotid gland acinic cell carcinoma. Eight years later, his daughter presented
at the age of 16 years with a nontender parotid gland mass that was excised
and found also to be acinic cell carcinoma. The histologic features of
both neoplasms were typical of acinic cell carcinoma.
While this may represent a coincidental event, the possibility that this
familial occurrence is a manifestation of common genetic or environmental
risk cannot be excluded.
Immunohistochemical Characterization of
Pancreatic Tumors Induced by Dimethylbenzanthracene in Rats
Ramon E. Jimenez, Kaspar Z'graggen, Werner Hartwig, Fiona Graeme-Cook,
Andrew L. Warshaw and Carlos Fernandez-del Castillo
From the Departments of Surgery and Pathology, Massachusetts General Hospital,
Harvard Medical School, Boston, Massachusetts
American Journal of Pathology. 1999;154:1223-1229
Courtesy PubMed/NCBI
Dimethylbenzanthracene (DMBA) induces
pancreatic adenocarcinomas in rats 9 months after carcinogen exposure,
with precursor lesions (tubular complexes) developing 1 month after initiation
of treatment. Because previous studies have suggested an acinar cell of
origin for these tumors, researchers investigated the expression pattern
of ductal, acinar, and islet cell markers in these cancers to gain insight
into their phenotype and cell of origin. For comparison, 5 human ductal
adenocarcinomas were also evaluated. Results are given.
Immunohistochemical Characterization of
Pancreatic Tumors Induced by Dimethylbenzanthracene in Rats
Ramon E. Jimenez, Kaspar Z'graggen, Werner Hartwig, Fiona Graeme-Cook,
Andrew L. Warshaw and Carlos Fernandez-del Castillo
From the Departments of Surgery and Pathology, Massachusetts General Hospital,
Harvard Medical School, Boston, Massachusetts
American Journal of Pathology. 1999;154:1223-1229
Dimethylbenzanthracene (DMBA) induces pancreatic adenocarcinomas in rats
9 months after carcinogen exposure, with precursor lesions (tubular complexes)
developing 1 month after initiation of treatment. Because previous studies
have suggested an acinar cell of origin for these tumors, we investigated
the expression pattern of ductal, acinar, and islet cell markers in these
cancers to gain insight into their phenotype and cell of origin. Pancreatic
neoplasms were induced in rats by implantation of DMBA into the head of
the pancreas. Lesions studied included 10 early tubular complexes (DMBA
for 2 weeks), 8 tubular complexes (DMBA for 1 month), and 10 adenocarcinomas
(DMBA for 9 months). Normal rat pancreas served as a control. For comparison,
5 human ductal adenocarcinomas were also evaluated. Immunohistochemistry
with ductal (keratin, cytokeratin 19, cytokeratin 20), acinar (chymotrypsin),
and islet (chromogranin A) cell markers was performed to analyze the tissues.
Rat tubular complexes and adenocarcinomas revealed strong expression of
keratin, cytokeratin 19, and cytokeratin 20 in the cytoplasm of all neoplastic
cells, absence of chymotrypsin, and rare immunoreactivity to chromogranin
A. Human adenocarcinomas showed strong expression of keratin and cytokeratin
19 in all neoplastic cells, expression of cytokeratin 20 in 5–20%
of cells, and absence of chymotrypsin and chromogranin A. Pancreatic adenocarcinomas
induced by DMBA in rats express markers consistent with a ductal phenotype,
as observed in human tumors. Ductal marker expression in early tumor stages
suggests a ductal cell of origin.
NCI Releases Results of Nationwide Study
of Radioactive Fallout from Nuclear Tests
Press Release
1:00pm EDT
Friday, August 1, 1997
NCI Press Office : (301) 496-6641
A press release announcing release of summary results from a study to
assess American’s exposure to radioactive iodine-131 fallout from
atmospheric nuclear bomb tests carried out at the Nevada Test Site in
the 1950s and 1960s. Depending on their age at the time of the tests,
where they lived, and what foods they consumed, particularly milk, Americans
were exposed to varying levels of I-131 for about two months following
each of the 90 tests.
(Note: This citation to be added in the future.)
Note: There is much more information on
this subject at the National Cancer Institute, including charts of calculated
radiation exposure. We will add these citations later.
A Message from a Downwinder
Posted to Downwinders’ Homepage
At website: pubpages.unh.edu
July 15, 1997
Letter from a patient with Acinic Cell Carcinoma, exposed to ionizing
radiation from nuclear testing. Both the patient and their sister developed
acinic cell carcinoma, which is unusual in itself. Patients physicians’
were convinced that the sisters got the cancer due to ionizing radiation
exposure. Both sisters developed the cancer as adults. But they had grown
up in Idaho, where there was suspected environmental radiation exposure.
Subsequent investigation revealed that the U.S. government had been doing
nuclear testing that likely was a factor in this and other cases of cancer,
as well as other health problems. Note: People who are not in the immediate
area of nuclear (or atomic) testing, but who may be exposed due to wind/weather
patterns are referred to as “Downwinders”.
(Note: We will be adding this citation in the future.)
Detection of p53 and histopathological classification
of skin tumours induced by halogen lamps in hairless mice.
D'Agostini F, Fiallo P, Di Marco C, De Flora S.
Institute of Hygiene and Preventive Medicine, University of Genoa, Italy.
Cancer Lett 1994 Nov 11;86(2):167-75
Courtesy of PubMed/NCBI
Skin lesions induced by exposure of three strains of female hairless mice
to the light emitted by uncovered halogen quartz lamps were subjected
to histopathological analysis. We examined 170 representative specimens
out of a total of 597 skin lesions, i.e. 38 out of 74 SKH-1 mice, 110
out of 472 MF-1 mice, and 42 out of 51 C3H mice. The results provided
evidence of various types of alterations, including preneoplastic changes,
such as epidermal hyperplasia, and benign tumours, such as papillomas,
as well as tumours with an increasing degree of malignancy, i.e., keratoacanthoma-like
tumours, appendage/basal tumours, actinic keratoses/carcinomas in situ,
and squamocellular carcinomas. SKH-1 was the most sensitive strain to
the far-ultraviolet wavelengths delivered by halogen lamps, as shown not
only by the shortest latency time and the highest multiplicity of skin
lesions but also by the highest frequency of malignant tumours. Some areas
of atypical melanocyte proliferation were only detected in C3H pigmented
mice. Eighty-two of the lesions excised from MF-1 mice were additionally
examined for p53 protein by immunohistochemical methods. Formalin-fixed,
paraffin-embedded sections and frozen sections were analyzed in parallel
by using polyclonal CM-1 antibody and monoclonal PAb240 antibody, respectively.
A positive response for p53 was only observed in squamocellular carcinomas,
and was related to the size of cancers; in fact, six out of 10 cancers
of 10-30 mm in diameter were positive, whereas all 16 cancers of 2-9 mm
in diameter were negative. All six positive squamocellular carcinomas
were detected by using the CM-1 antibody, which recognizes both wild-type
and mutant forms of p53 protein, and five of them were also positive with
the PAb 240 antibody, which only recognizes the mutant form. Thus, p53
mutation appears to be a late event in the development of halogen-induced
skin tumours in hairless mice, requiring a severe degree of malignancy
and an advanced stage of the neoplastic mass growth.
Potent carcinogenicity of uncovered halogen lamps
in hairless mice.
D'Agostini F, De Flora S.
Institute of Hygiene and Preventive Medicine, University of Genoa, Italy
Cancer Res 1994 Oct 1;54(19):5081-5.
Courtesy of PubMed/NCBI
Uncovered halogen quartz lamps, which are potently genotoxic both in prokaryotic
and human cells due to the emission of far-UV radiation (UVB and UVC),
were assayed for carcinogenicity in three strains of hairless mice (SKH-1,
MF-1, and C3H) of both sexes. As assessed in 5 independent experiments,
no spontaneous skin tumor was observed, even after more than 2 years,
in 49 animals used as unexposed controls or in 29 animals exposed to halogen
lamps equipped with a common glass cover. In contrast, almost all of the
185 mice exposed to the light emitted by low-voltage (12 V) and low-power
(50 W) tungsten bulbs, equipped with dichroic diffusers, contracted multiple
skin tumors of various histological type, both benign and malignant. Tumors
were induced over a range of illuminance levels (1,000, 3,333, 5,000,
and 10,000 lux) and daily exposure times (1.5, 3, 6, and 12 h). The tumor
latency times were quite short and significantly correlated with the daily
exposure times, as well as with the square of the distance (46-194 cm)
from the illumination source. A carcinogenic effect was even observed
when exposure was discontinued well before the appearance of skin lesions.
Both in vitro genotoxicity data and animal carcinogenicity data support
the view that the light emitted by uncovered halogen lamps, to which an
enormous number of individuals are exposed, may pose carcinogenic risks
to humans. Without renouncing the benefits of this modern illumination
system, UV-blocking devices should be compulsory.
Erythema induced by quartz-halogen sources.
Cesarini JP, Muel B.
INSERM, Fondation A. de Rothschild, Paris, France.
Photodermatol 1989 Oct;6(5):222-7
The erythemal effect of 100-W quartz-halogen sources, previously predicted
from radiation measurements, was directly measured on humans at a distance
of 10 cm. Minimal erythema was produced in 15 min for skin type I. These
data show that normal use of a desktop lamp should not usually lead to
erythema in one day, but that long-term effects cannot be ignored, because
for lifetime use at work, the relative risk for squamous cell carcinoma
on the back of the hands is 3.4.
Major salivary gland carcinoma. Descriptive epidemiology
and survival of 498 patients
Spitz MR, Batsakis JG
Arch Otolaryngol; 110(1):45-9 1984
Courtesy of PubMed/NCBI
A retrospective chart review study was conducted on 498 patients with
histopathologically confirmed carcinoma of the major salivary glands to
ascertain the potential risk factors and to abstract the clinicopathologic
and survival data. The distribution of histologic classification varied
by race, sex, and history of benign salivary gland lesion (37 patients).
Of the 57 patients who had a history of radiation exposure, 49 patients
had been irradiated in a field encompassing the salivary gland area. Sixty-six
patients had had a prior primary cancer. Of 43 instances of previous skin
cancer, 37 occurred in male patients. The rationale for a possible relationship
between cutaneous neoplasms and salivary carcinoma is explained embryologically
and histogenetically. Tumor histology, anatomic site, race, and sex were
important predictors of survival.
To come in the future:
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