Content uploaded by Georgi Tchernev
Author content
All content in this area was uploaded by Georgi Tchernev on Feb 20, 2024
Content may be subject to copyright.
МЕДИЦИНСКИ ПРЕГЛЕД, 2024, 60 (3) 67
2211
1Onkoderma – Clinic for Dermatology, Venereology and Dermatologic Surgery
2Department of Dermatology and Venereology, Medical Institute of Ministry of Interior – Sofia
2211
1Онкодерма – Клиника по дерматология, венерология и дерматологична хирургия
2Катедра по дерматология и венерология, Медицински институт на МВР – Софияa
The contribution of dermatologists to global oncology also remains largely attrib-
utable to the incidental identification or clinicopathologic correlations between
the intake of nitrosamine-contaminated drugs and the subsequent generation of
melanomas and keratinocytic cancers. The slow and gradual identification of an
increasing number of nitrosamine containing drugs, and their subsequent associ-
ation with the development of heterogeneous forms of skin cancer, underlies the
newly introduced concept, now also known as drug-induced nitrosogenesis/car-
cinogenesis or that of skin cancer pharmaco-oncogenesis. Of undoubted interest
is also the fact that the intake of mono- or polycondaminated drugs in the context
of polymorbidity could (according to recent analyzes) also be controlled and not
only be sporadic or unexplained. It is this that necessitates, albeit to some extent
according to some, the speculative claim that cancer could be controlled and ni-
trosamines are genetic weapon for controlled cancer causation. The resolution of
this dilemma could be accomplished through several non-negligible steps such
as 1) accurate cataloguing of nitrosamines or their derivatives on each and every
drug package – in terms of availability and concentration, 2) certificates of drug
purity on each batch, 3) independent additional monitoring of nitroso incidence
once the certificates are formalized, 4) an official online database for catalogu-
ing the side effects of nitroso-contaminated drugs (accessible and transparent
to end-users, manufactured; or 5) complete elimination of nitroso components
from medicinal preparations. Oncopharmacogenesis/pharmaco-oncogenesis of
skin cancer is a concept that is key, enigmatic and without analogue. It should
not be confused with concepts such as pharmacogenetics/ pharmacogenomics.
The reason this concept (onco-pharmacogenesis/pharmaco-oncogenesis) came
up was defined by the FDA and its enigmatic revelations of nitrosocontamination
(cancer related nitrosogenesis) of drug production back in 2018.
Nitrosogenesis, skin cancer, melanoma, polycontamination, NDSRIs, nitrosamines
Address for correspondence: Prof. Georgi Tchernev, DM, e-mail: georgi_tchernev@yahoo.de,
рhone: +359 885 588 424
Приносът на дерматолозите към световната онкология до голяма степен се
дължи и на случайното идентифициране на клинико-патологичните корелации
между приема на замърсени с нитрозамини лекарства и последвалото въз-
никване на меланоми и кератиноцитни форми на рак. Бавното и постепенно
идентифициране на все по-голям брой нитрозамин-съдържащи лекарства и
последващата връзка с развитието на хетерогенни форми на рак на кожата,
е в основата на нововъведената концепция, която понастоящем е известна и
като лекарствено медиирана нитрозогенеза/канцерогенеза, или като фармако-
68 МЕДИЦИНСКИ ПРЕГЛЕД, 2024, 60 (3)
онкогенеза на рака на кожата. Безспорен интерес представлява и фактът, че
приемът на моно- или поликонтаминирани лекарства в контекста на полимор-
бидността би могъл (според последните анализи) да бъде и контролиран, а
не само спорадичен или необясним. Именно това налага, макар и до извест-
на степен (според някои учени) донякъде и спекулативното твърдение, че рак-
ът би могъл да бъде контролиран, а нитрозамините са генетично оръжие за
контролирано провокиране на рак. Разрешаването на тази дилема би могло
да се осъществи чрез няколко немаловажни стъпки, като например: 1) пре-
цизно каталогизиране на нитрозамините или техните производни върху всяка
опаковка на лекарството – по отношение на наличността и концентрацията,
2) сертификати за чистота на лекарството върху всяка партида, 3) независим
допълнителен мониторинг на честотата на разпространение на нитрозамините,
след като сертификатите бъдат официализирани, 4) официална онлайн база
данни за каталогизиране на страничните ефекти на замърсените с нитроза-
мини лекарства (достъпна и прозрачна за крайните потребители, произведена
или 5) пълно премахване на нитрозокомпонентите от лекарствените препарати.
Онкофармакогенеза/фармакоонкогенеза на рака на кожата е понятие, което е
ключово, енигматично и без аналог. То не би следвало да се бърка с понятия
като фармакогенетика/фармакогеномика. Причината за появата на това поня-
тие (онкофармакогенеза/фармакоонкогенеза) се определя от FDA и нейните
енигматични разкрития за нитрозамърсяване (медиираща рака нитрозогенеза)
в рамките на производството на лекарства още през 2018 г.
нитрозогенеза, рак на кожата, меланом, поликонтаминация, NDSRIs, нитрозамини
Aдрес за кореспонденция: Проф. д-р Георги Чернев, e-mail: georgi_tchernev@yahoo.de, тел.: +0 885 588 424
The nitrosogenesis of cancer is a concept that
has recently been introduced as a definition in medi-
cine, mainly in the context of skin cancer [1]. Nitroso-
genesis is inextricably linked to carcinogenesis, and
both concepts have been moving forward over the
years ʺhand in handʺ [2].
The concept of exogenously induced, drug-in-
duced nitrosogenesis/onco-pharmacogenesis/ phar-
maco-oncogenesis refers to either primarily the intake
of nitrosamines in drugs and the subsequent genera-
tion of skin cancers like melanoma [3-5] or non-mel-
anoma forms of skin cancer [6-9], or the concurrent/
staged occurrence of both [10, 11].
Various forms of cancer could arise after 1) in-
take of drugs potentially or actually contaminated with
nitrosamines [12], but also 2) inhalation or 3) direct
contact (?) with the skin in oil refinery workers [13].
The link is mainly between contact with a particular
carcinogen/mutagen/nitrosamine and the subsequent
generation of melanomas, but not only. Regardless of
the form, in which they are taken or come into contact
with the body, certain nitrosamines are capable of in-
ducing melanomas [3-5, 13]. The organ-specific ac-
tion of nitrosamines has been known since the 1990s,
but remains poorly thematized today [14].
What has been mentioned so far does not exclude
the occurrence of other forms of cancer – in the con-
text of, for example, inhalation of nitroso derivatives
with cigarette smoke [15-18], oral intake with water,
beer, food [19], or de novo occurrence in the stomach
after intake of amine- or nitrosamine-rich food [20].
The de novo activation of nitrosamines after me-
tabolization in the liver is not to be overlooked and is
difficult to identify (over 300 nitrosamines) and cata-
logue, requiring modified assays to capture potential
carcinogenic activity [21, 22]. More than 300, even
400 nitrosamines are known, and their carcinogenic
effects on the human genome are currently under
investigation [23]. In all likelihood, this action is not
classified as beneficial but rather as mutagenic, car-
cinogenic or cancer-causing. As skin cancer appears
to be another peculiar model of the action of nitrosa-
mines within drug intake [1, 3, 4, 8].
The fact that certain batches of drugs such as
sartans, in certain geographical regions (Turkey),
could be unaffected by contamination suggests indi-
rectly that this contamination could be cleaned up in a
controlled manner [24]. However, it is also indicative
of the following: this contamination could probably
also be controlled/time-targeted and regulated, which
could in practice also turn it into a kind of genetic
МЕДИЦИНСКИ ПРЕГЛЕД, 2024, 60 (3) 69
weapon ʺfor quiet destructionʺ [25, 26]. The genetic
sequencing/profiling of human genome weaknesses
(even through a single blood sample) in a particular
race and/or zone does not preclude the subsequent
precise targeting of an organism or a particular sys-
tem within it by genome modifiers/nitrosamines at a
later stage [25, 26]. The subject matter sounds more
like science fiction, but it is not to be ignored.
The tissue-specific action of these mutagens/
carcinogens/nitrosamines is currently far from the
focus of objective truth, but presumably it is only
a matter of time before this becomes a formalized
reality. In fact, there is a problem concerning the
controlled release of tissue-specific genome modi-
fiers or carcinogens/so-called nitrosamines, which
are in all likelihood at least partly responsible for
the cancer pandemic of the 21st century [27]. Ni-
trosamines – a silent weapon of mass, permanent,
controlled and silent destruction of certain popula-
tion and at certain geographical region?
Carcinogens that have been in the forced toler-
ance stage for decades, but currently declared as
forced availability in drugs taken by over 5 billion
daily [28].
Contact with nitrosamines has also been associ-
ated for decades with the subsequent occurrence of
cancer in rodents under experimental conditions [29].
In the middle of the last century, an English collective
made enigmatic discoveries that conclusively proved
the carcinogenic role of a certain type of nitrosamines
in the generation of cancer in rats [30]. These can-
cers were again shown to be tissue specific and con-
cerned liver cancer and kidney cancer after N-Nitros-
odimethylamine intake [29, 31].
Strangely how and why, a French team, albeit 60
years later, also revealed a link between NDMA intake
and melanoma and liver cancer – 10% of patients de-
veloped these two types of tumors [32]. Interesting in
this study is the fact that they followed patients with
NDMA-contaminated valsartan alone and the subse-
quent development of neoplasms [32]. It would be
logical to ask the question: ʺWhat would be the % of
neoplasms in a trial of valsartan contaminated with a
heterogeneous type of nitrosamines/NDSRIs? Were
the patients taking any other medications and are the
latter catalogued in the FDA list of April 2023 for poly-
contaminated drugs?ʺ. In order to detect valsartan
products contaminated with NDMA only, contamina-
tion with any type of nitrosamines should have been
excluded? Have any such tests been carried out and
what is the percentage positive for other types of ni-
trosamines – why is this not thematized? Assuming
this percentage was negative or less than 10%, it
would be formalized as a significant contribution of
the publication. The absence of any data on the occa-
sion is indicative of the generalized assumption that
the percentage of valsartan contaminated with other
nitrosamines is probably much higher than 10% and
therefore remains unformalized, unthematized even.
It is this one-sidedness of the information shared
[32] that is at the root of the doubts constantly raised
about the reliability and objectivity of the data.
Strange how, but 70 years later, some of the most
potent carcinogens, turn out to be an integral part of
the drug menu of more than 5 billion patients world-
wide and this is documented even by the FDA as nor-
mal [28]. And no one knows how they came about,
with regulators seeking to keep nitrosamines present
in medicines, and a ʺridiculous attemptʺ to block/neu-
tralize their carcinogenic effect with vitamin C intake,
for example [22, 33].
It remains an open question 1) whether the pro-
duction from India and China will continue to be ad-
vertised as ʺMade in EUʺ when packaged in Europe
and 2) whether the thirst for cheap nitroso produc-
tion will overcome the desire to actually fight cancer.
This decision should be decided by regulators and
imposed on manufacturers.
Nitrosogenesis concerns almost all known forms
of cancer, and these links are still ignored by many of
the world‘s established publications. The information
curtain allows the global statistics regarding cancer
to grow at breakneck speed and provides 1.4 trillion a
year to the manufacturers in the face of Big Pharma
[34]. As this fact is only made possible by a kind of
umbrella of regulators and is termed: forced zero tol-
erance of cancer inducing mutagens.
It is the FDA organization, whose objectivity
sometimes allows the spark of truth to shine for a mo-
ment, often ʺquickly extinguished, like a falling starʺ.
Allowing the flame of truth to smolder remains to be
guaranteed only by the morality of clinicians and the
formalization of objective truth, ensuring full transpar-
ency of clinical data and hence the possibility of cor-
rect decisions.
Decisions that should be binding on both regula-
tors and producers. The hegemony of the latter two
must be definitively removed, as their insufficiency
has been definitively proven.
The mono and/or polycontamination of drugs
with nitrosamines is an undeniable and alarming fact
that has been present for at least 30 (if not more)
years according to the manufacturers‘ own informa-
МЕДИЦИНСКИ ПРЕГЛЕД, 2024, 60 (3)
tion [1, 3, 6-9]. This contamination provides a per-
manent, continuous and daily contact of the human
organism with some of the most potent genome mod-
ifiers, the so-called nitrosamines or NDSRIs [1, 3].
The Sleepwalking of the contamination is accom-
panied by the surprising prolongation of its forced
presence years after its detection (2018-2024) [28].
And so far. To the detriment of the global health map
and ʺin aid of cancer incidenceʺ. This strongly sup-
ports the (hypo)thesis of cartel agreements between
regulators and drug market manufacturers.
Exogenous drug-mediated nitrosogenesis is one
of the important reasons for the possible targeting
of certain acquired mutations that could possibly be
controlled in terms of time, place and target group.
Although speculative, this thesis remains floating
in time and space. Elimination of carcinogens from
drugs is entirely possible even in the short term;
however, this remains in all likelihood undesirable by
each of the entities mentioned: regulators and manu-
facturers. Delaying final decisions in this direction is
throwing fine dust in the eyes of others, while prob-
ably backroom deals continue to flow with full force.
The question remains open: what prevents compa-
nies from betting on production that has been found
to be uncontaminated? The choice is effectively be-
tween contaminated cheap production and controlled
expensive production, with smaller, foreseeable prof-
its and lower cancer rates overall?
Cross-analysis of various statistical databases
such as those concerning the worldwide incidence of
cancer, that of melanoma and of keratinocytic can-
cers, related to pathogenetic factors currently known
to the medical community, has been able to: 1) identify
new etiopathogenetic factors (such as nitrosamines),
2) challenge to a large extent also the relevance of
some old pathogenetic factors such as for instance
solar radiation. It is these analyses that establish the
significant role of the new mutagens ubiquitously dis-
tributed with drugs: the nitrosamines.
Globocan‘s prognostic data for the year 2040
promise, despite and contrary to medical progress,
a dramatic increase in cancer incidence worldwide of
nearly 50% [35]. The incidence of melanoma also re-
mains startling and makes no significant difference in
this regard [36]. But what does this mean in practice?
Standard prevention regarding skin cancer has
been largely and poorly effective, preventing mela-
noma from being ʺkept in chessʺ [3]. This in turn con-
ditions the search for alternatives to further elucidate
its pathogenesis. These alternatives are directed en-
tirely at a new, unpredictable, until recently unknown,
uninvited guest on the patientsʼ medication menu –
nitrosamines [8]. Unfortunately, this uninvited guest
is also present in food, drinks, cigarettes, and water
[37-39]. The widespread occurrence of these carcin-
ogens should not discourage its gradual and timely
elimination from medications.
However, the contamination of the drug market
with these mutagens remains the biggest scourge of
global health at the moment, and the explanation for
this availability is shrouded in mystery to this day.
It is unclear – why do regulatory agencies refuse
to stop contaminated production from being distrib-
uted? It is also unclear – why do they still not require
manufacturers to label the exact concentration of mu-
tagens contained on the packaging or prescription of
a drug? Is this not about controlling cancer and its
occurrence? A time-gainer, but not only that?
The enforcement regimens created to tolerate
certain concentrations of carcinogens with drugs
(due to the ridiculous explanation of no alternative)
[28, 40], are also the most direct evidence of how the
rush to profits by pharmaceutical companies and the
powerlessness of regulators, are proving to be more
of a priority and desirable, and global health is being
pushed out of focus [8].
This contaminated intake is also most often con-
ditioned as polymedication within polymorbidity [3, 6,
7-9]. It remains to date uncontrolled, unrecognized
and generating skin cancer, but not only [10, 12].
De facto, it concerns the intake of carcinogens
within the framework of polymedication, which could
in fact justify the available frightening predictions ac-
cording to Globokan, referred to 2040 [35]. To date,
there is not even a single worldwide follow-up that
takes into account 1) polymedication in the context
of officially declared polycontamination with carcino-
gens/nitrosamines known for decades and relates it
to 2) the generation of a specific cancer form, accord-
ing to relevant statistics.
Herein lies the key to the genesis of skin cancer
– and cancer in general – globally: according to initial
preliminary (as yet unannounced), currently unpub-
lished data, the percentage of new cancers world-
wide following the intake of drugs that are catalogued
in the FDA lists of potentially/actually contaminated
drugs announced in 2023 is over 80-85%. And this
applies with full force to certain geographic regions.
Serious attention should be paid to a new con-
cept – skin cancer related pharmaco-oncogenesis/
onco-pharmacogenesis, which concerns the intake of
drugs containing nitrosamines that are not declared
as officially present.
The so-called daily tolerable intakes for certain
carcinogens/mutagens/nitrosamines could be (and in
МЕДИЦИНСКИ ПРЕГЛЕД, 2024, 60 (3) 71
practice are) exceeded many times over, but these
remain undisclosed to patients and clinicians even
at present. The reason for their non-disclosure is the
fact that 1) nitrosamine concentrations are elevated,
and 2) seeking direct responsibility at any level is dif-
ficult to impossible, especially when official data on
any availability is lacking.
Absolutely irrelevant remains the circumstance
and at the same time unsolvable dilemma: 1) whether
the data on the 20-fold elevated concentration of ni-
trosamines is due to contamination within 1.1) mono-
medication or 1.2) the 10-fold elevated concentration
with nitroso derivatives, for example, is a reality, but
within polymedication. And probably over a period
of more than 50 years. Both states of contamination
(mono/poly) are associated with the generation of
skin cancer and remain hidden to the societal mind-
set that would even welcome them within the frame-
work of globalization and murderous growth rates: of
anything and everything at any cost; however – let it
be today, even if it is a drug initiated death, within a
controlled intake of carcinogens.
Clinicopathologic correlations identified and
thematized only by clinicians are indicative of such
availability, even when concentrations of nitrosa-
mines/NDSRIs are not being formalized or even
thematized [41-44].
However, this formalization has been slow to take
off and the objectivity of the data has been assured
not by regulators and manufacturers but by clinicians
[45-49]. And it is, remains and will be murderously
indicative.
Exogenously mediated nitrosogenesis/onco-
pharmacogenesis/pharmaco-oncogenesis remains
to this day the most serious (in some people‘s view
still likely) dealer of programmed, controlled death. Its
elimination should be seen as a priority. At all levels
and at all costs.
1. Tchernev G, Kordeva S. Nitrosogenesis of skin (human) can-
cer – the hidden truth of a neverending story: nitrosamine con-
tamination in olmesartan, valsartan and hct as main risk fac-
tor for the development of keratinocyte cancer. Georgian Med
News. 2023 Apr;(337):63-67.
2. Magee PN, Barnes JM. Carcinogenic nitroso compounds.
Adv Cancer Res. 1967;10:163-246. doi: 10.1016/s0065-
230x(08)60079-2.
3. Tchernev G. Nitrosogenesis of cutaneous melanoma: simul-
taneously development of primary cutaneous thick melanoma
of the breast, thin melanoma/dysplastic mole of the back dur-
ing parallel intake of bisoprolol, amlodipine and valsartan/ hct:
nitrosamine polycontamination in the multimedication as the
most powerful skin cancer trigger. Georgian Med News. 2023
Jun;(339):83-88.
4. Tchernev G. Nitrosogenesis, antidepressants and the sertralin
induced nevus associated cutaneous melanoma: the ndma/
nnk (ndsris) contamination as most potent melanoma inductors:
alea iacta est. Georgian Med News. 2023 Sep;(342):47-53.
5. Tchernev G. Neighbouring melanomas and dysplastic nevus
developing simultaneously after candesartan intake: nitrosa-
mine contamination/ availability as main cause for skin can-
cer development and progression. Georgian Med News. 2023
Mar;(336):104-107.
6. Tchernev G. Nitrosamine contamination within cardiac multi-
medication – sartans (valsartan), calcium channel blockers
(amlodipine and nifedipine), and antiarrhythmics (propafenone)
as a significant factor in the development and progression of
multiple keratinocytic cancers: advancement rotation flap for
keratoacanthoma of the upper lip and undermining surgery for
bcc of the shoulder as an optimal dermatosurgical approach.
Georgian Med News. 2023 Sep;(342):152-155.
7. Tchernev G. Nitrosogenesis lessons from dermatologists-
nitrosamines/ ndsris contamination of the polimedication in
polimorbid patients as the most powerful skin cancer induc-
tor: double hatchet flap for scc of the scalp occurring during
treatment with valsartan/hydrochlorothiazide and lercanidipine.
Georgian Med News. 2023 Sep;(342):74-79.
8. Tchernev G. The nitrosamine contamination in beta blockers
(bisoprolol/metoprolol), ace inhibitors (lisinopril/perindopril),
thiazides diuretics (hct), calcium channel blockers (amlodipine/
felodipine), sartans (candesartan) and тhe subsequent skin
cancer development and progression: apocalypse now. Geor-
gian Med News. 2023 Apr;(337):138-145.
9. Tchernev G, Lozev I, Ivanov L. Morpheaform bcc of ala nasi:
a successful dermatosurgical approach by transposition flap
from the adjacent area. contamination of venlafaxine, biso-
prolol and olanzapine with nitrosamines/ndsris: the most likely
cause of skin cancer development and progression. Georgian
Med News. 2023 Sep;(342):26-29.
10. Tchernev G. Nitrosamines in commonly prescribed antihy-
pertensives and the (un)controlled drug-induced skin cancer:
simultaneous development of cutaneous melanoma and multi-
ple bcc after concomitant administration of bisoprolol and furo-
semide. Georgian Med News. 2023 Sep;(342):149-151.
11. Tchernev G. А flavour of death: perindopril induced thick
melanoma and bcc of the back. potential role of the generic
substance or/-and possible nitrosamine contamination as
skin cancer key triggering factors. Georgian Med News. 2023
Mar;(336):123-125.
12. Tchernev G. Nitrosogenesis of skin cancer: the nitrosamine
contamination in the calcium channel blockers (amlodipine),
beta blockers (bisoprolol), sartans (valsartan/losartan), ace
inhibitors (perindopril/enalapril), tricyclic antidepressants (me-
litracen), ssris (paroxetine), snris (venlafaxine) and metformin:
the most probable explanation for the rising skin cancer inci-
dence. Georgian Med News. 2023 Jun;(339):24-32.
13. Bell CM, Jenkinson CM, Murrells TJ, et al. Aetiological factors
in cutaneous malignant melanomas seen at a UK skin clinic.
J Epidemiol Community Health. 1987 Dec;41(4):306-11. doi:
10.1136/jech.41.4.306.
14. Pool BL, Schmezer P, Tompa A, Brendler SY. Organ spe-
cific genotoxicity and carcinogenicity. Prog Clin Biol Res.
1990;340D:33-41
15. Auschwitz E, Almeda J, Andl CD. Mechanisms of E-Ciga-
rette Vape-Induced Epithelial Cell Damage. Cells. 2023 Oct
31;12(21):2552. doi: 10.3390/cells12212552.
МЕДИЦИНСКИ ПРЕГЛЕД, 2024, 60 (3)
16. Shehata SA, Toraih EA, Ismail EA, et al. Environmental Toxi-
cants Exposure, and Lung Cancer Risk. Cancers (Basel). 2023
Sep 12;15(18):4525.
17. Bracken-Clarke D, Kapoor D, Baird AM, et al. Vaping and
lung cancer - A review of current data and recommenda-
tions. Lung Cancer. 2021 Mar;153:11-20. doi: 10.1016/j.lung-
can.2020.12.030. Epub 2021 Jan 2.
18. Etemadi A, Poustchi H, Chang CM, et al. Exposure to polycy-
clic aromatic hydrocarbons, volatile organic compounds, and
tobacco-specific nitrosamines and incidence of esophageal
cancer. J Natl Cancer Inst. 2023 Oct 19:djad218.
19. https://www.efsa.europa.eu/en/news/nitrosamines-food-raise-
health-concern
20. Song P, Wu L, Guan W. Dietary Nitrates, Nitrites, and Nitrosa-
mines Intake and the Risk of Gastric Cancer: A Meta-Analysis.
Nutrients. 2015 Dec 1;7(12):9872-95. doi: 10.3390/nu7125505.
21. Li Y, Hecht SS. Metabolic Activation and DNA Interactions of
Carcinogenic N-Nitrosamines to Which Humans Are Common-
ly Exposed. Int J Mol Sci. 2022 Apr 20;23(9):4559.
22. https://www.chemistryworld.com/news/addressing-the-saga-
of-nitrosamine-contamination-in-drugs/4018123.article
23. Ruepp R, Frötschl R, Bream R, et al. The EU Response to the
Presence of Nitrosamine Impurities in Medicines. Front Med
(Lausanne). 2021 Nov 19;8:782536.
24. Öncü T, Yüksel B, Binay E, Şen N. LC-MS/MS Investiga-
tion of nitrosamine impurities in certain Sartan group me-
dicinal products available in Istanbul, Türkiye. Ann Pharm
Fr. 2023 Aug 9:S0003-4509(23)00079-2. doi: 10.1016/j.phar-
ma.2023.08.002. Epub ahead of print.
25. https://nonproliferation.org/op-52-scientific-risk-assessment-
of-genetic-weapons-systems/
26. Berg F, Kappler S. In Ciottone‘s Disaster Medicine (Third Edi-
tion) 2024; Chapter Future Biological and Chemical Weapons:
520-530.
27. https://www.kcl.ac.uk/news/urgent-action-required-for-the-uk-
and-us-to-tackle-the-global-cancer-epidemic
28. https://www.fda.gov/regulatory-information/search-fda-guid-
ance-documents/updated-information-recommended-accepta-
ble-intake-limits-nitrosamine-drug-substance-related
29. Magee PN, Barnes JM. The production of malignant primary
hepatic tumours in the rat by feeding dimethylnitrosamine. Br J
Cancer. 1956 Mar;10(1):114-22.
30. MAGEE PN, BARNES JM. The experimental production of
tumours in the rat by dimethylnitrosamine (N-nitroso dimeth-
ylamine). Acta Unio Int Contra Cancrum. 1959;15(1):187-90.
31. MAGEE PN, BARNES JM. Induction of kidney tumours in
the rat with dimethylnitrosamine (N-nitrosodimethylamine). J
Pathol Bacteriol. 1962 Jul;84:19-31.
32. Mansouri I, Botton J, Semenzato L, et al. N-nitrosodimethyl-
amine-Contaminated Valsartan and Risk of Cancer: A Nation-
wide Study of 1.4 Million Valsartan Users. J Am Heart Assoc.
2022 Dec 20;11(24):e8067. doi: 10.1161/JAHA.122.026739.
Epub 2022 Dec 19.
33. Tuesuwan B, Vongsutilers V. Nitrosamine Contamination in
Pharmaceuticals: Threat, Impact, and Control. J Pharm Sci.
2021 Sep;110(9):3118-3128. doi: 10.1016/j.xphs.2021.04.021.
Epub 2021 May 11.
34. https://www.statista.com/statistics/263102/pharmaceutical-
market-worldwide-revenue-since-2001/
35. Sung H, Ferlay J, Siegel RL, et al. Global Cancer Statistics
2020: GLOBOCAN Estimates of Incidence and Mortality
Worldwide for 36 Cancers in 185 Countries. CA Cancer J Clin.
2021 May;71(3):209-249. .
36. Arnold M, Singh D, Laversanne, et al. Global Burden of Cuta-
neous Melanoma in 2020 and Projections to 2040. JAMA Der-
matol. 2022 May 1;158(5):495-503.
37. Lin JK. Nitrosamines as potential environmental carcinogens in
man. Clin Biochem. 1990 Feb;23(1):67-71.
38. Park JE, Seo JE, Lee JY, Kwon H. Distribution of Seven N-
Nitrosamines in Food. Toxicol Res. 2015 Sep;31(3):279-88.
doi: 10.5487/TR.2015.31.3.279. Erratum in: Toxicol Res. 2018
Oct;34(4):371.
39. https://www.efsa.europa.eu/en/news/nitrosamines-food-raise-
health-concern
40. https://www.fda.gov/drugs/drug-safety-and-availability/fda-
updates-and-press-announcements-angiotensin-ii-receptor-
blocker-arb-recalls-valsartan-losartan
41. Nardone B, Majewski S, Kim AS, et al. Melanoma and Non-
Melanoma Skin Cancer Associated with Angiotensin-Con-
verting-Enzyme Inhibitors, Angiotensin-Receptor Blockers
and Thiazides: A Matched Cohort Study. Drug Saf. 2017
Mar;40(3):249-255.
42. Sipahi I. Risk of cancer with angiotensin-receptor blockers
increases with increasing cumulative exposure: Meta-re-
gression analysis of randomized trials. PLoS One. 2022 Mar
2;17(3):e0263461.
43. Azoulay L, St-Jean A, Dahl M, et al. Canadian Network for Ob-
servational Drug Effect Studies (CNODES) Investigators. Hy-
drochlorothiazide use and risk of keratinocyte carcinoma and
melanoma: A multisite population-based cohort study. J Am
Acad Dermatol. 2023 Aug;89(2):243-253.
44. Mehlan J, Ueberschaar J, Hagenström K, et al. The use of
HCT and/or ACE inhibitors significantly increases the risk of
non-melanotic skin cancer in the periocular region. Graefes
Arch Clin Exp Ophthalmol. 2022 Aug;260(8):2745-2751.
45. Mansouri I, Botton J, Semenzato L, et al. N-nitrosodimethyl-
amine-Contaminated Valsartan and Risk of Cancer: A Nation-
wide Study of 1.4 Million Valsartan Users. J Am Heart Assoc.
2022 Dec 20;11(24):e8067.
46. Etemadi A, Poustchi H, Chang CM, et al. Exposure to polycyclic
aromatic hydrocarbons, volatile organic compounds, and tobac-
co-specific nitrosamines and incidence of esophageal cancer. J
Natl Cancer Inst. 2023 Oct 19:djad218.
47. Okafor S, Muzaffar J, Jang D, et al. Nasopharyngeal Carci-
noma: Case Presentation and Literature Review of Treatment
Innovation with Immunotherapy. J Neurol Surg Rep. 2023 Sep
27;84(3):e113-e115.
48. Shehata SA, Toraih EA, Ismail E, et al. Vaping, Environmental
Toxicants Exposure, and Lung Cancer Risk. Cancers (Basel).
2023 Sep 12;15(18):4525.
49. Sun Y, Jiang B, Wang X, et al. Occurrence of N-nitrosodimeth-
ylamine in roasted Alaska pollock fillets during processing and
storage and preliminary cancer risk assessment. J Sci Food
Agric. 2023 Nov;103(14):6940-6946.
Постъпила за печат на 2 февруари 2024 г.