APPENDIX 1
Supplementary memorandum by the Department
of Health (TB 1A)
When officials from the Department of Health
gave evidence to the Committee on 18 November Members of the Committee
asked for further information on several points. This further
memorandum consists of notes on the following:
(1) research on the carcinogenicity of different
elements of tobacco smoke;
(2) research commissioned from the Laboratory
of the Government Chemist (LGC);
(5) societal costs of smoking;
(6) note on the legal status of the control
mechanism for tobacco and its regulation.
The Department will of course endeavour to respond
to any further enquiries and requests from the Committee.
1. DEPARTMENT
OF HEALTH
RESEARCH INTO
THE CARCINOGENICITY
OF DIFFERENT
CONSTITUENTS OF
TOBACCO SMOKE
1. The Department has not done any such
research. However, many studies have been carried out by others,
and the results published in the scientific literature.
2. The Department has funded the Laboratory
of the Government Chemist (LGC) to carry out testing of cigarettes
and other tobaccos for the presence of a variety of toxic components,
many of which will be recognised carcinogens (eg benzene, polycyclic
aromatic hydrocarbons). For further details of this research see
below. The LGC is not involved in the assessment of the carcinogenicity
of these compounds.
3. The Tobacco Products Research Trust (TPRT)
was involved in research investigating the health effects of modified
tobacco products (ie those with lowered yields of tar, nicotine
etc) but not specifically looking at cancer, other than the overall
incidence of cancers over time. It did not associate cancer incidence
with any particular compounds contained within the smoke.
4. Officials were asked about which aspect
of the chemical structure of nitrosamine is the carcinogen. It
is not possible to say that a particular part of this chemical
is responsible for carcinogenicity (and therefore infer that removal
of that part will reduce or remove the effect). It would require
removal of the whole compound to reduce/remove the effect.
2. DETAILS OF
LGC RESEARCH
5. The LGC carries out an ongoing programme
of research for the Department of Health. This comprises the testing
programme of cigarettes to ascertain their yields of tar, nicotine
and carbon monoxide and other research as commissioned within
an overall annual budget of approximately £540,000.
6. Recent commissioned research includes:
— Survey of tobacco-specific nitrosamines
in mainstream and sidestream cigarette smoke. Boardman MC &
Darrall KG. This survey determined the yields of those nitrosamines
specific to tobacco. Unpublished report to Department of Health
1994.
— Determination of polycyclic aromatic
hydrocarbons (PAHs) in mainstream smoke. This work was to examine
the effect of the tar reduction that has taken place over recent
years on the levels of 10 selected PAHs. Samples used were manufactured
and hand rolled cigarettes. The overall spectrum of PAHs seems
to be little changed and there is little variation between different
brands. Unpublished report to Department of Health, December 1996.
— Nitric oxide yields of cigarettes.
This was a follow up survey to those conducted in the 1980's.
Although average tar yields have fallen by 15-21 per cent since
the two previous surveys there was a corresponding increase in
average NO yields ranging from 28 per cent-51 per cent. There
have been changes in cigarette testing methodology in the intervening
years but these are unlikely to account for the increases in the
NO yields which are considered to be genuine. The most likely
explanation is the increase in the nitrate level of the Virginia
tobacco in that time. Brands manufactured from Burley tobacco
have lower yields of NO now, with corresponding decreased nitrate
levels. Report to Department of Health—June 1998. Publication
under consideration.
— Mainstream smoke yields of small
cigars and RYO tobacco—determination of PAHs. This work
analysed 24 brands of small cigars and RYO cigarettes as a follow
up to earlier work. There is, in general, a linear relationship
between tar yields and benzpyrene yields in small cigars, much
as is seen with cigarettes. But there is evidence that the smoke
from small cigars may be more carcinogenic than that from cigarettes,
since it contains higher levels of the more potent PAHs. Unpublished
report to Department of Health. August 1998.
— Mainstream smoke yields of small
cigars—determination of benzene and associated volatile
organic compounds. This followed an earlier report in 1996 analysing
yields in cigarettes. In general the cigar yields of the volatile
analytes are proportional to the tar yield. However, average benzene
levels are twice those in cigarette smoke. Unpublished report
to Department of Health, September 1998.
— Determination of benzene and associated
volatile compounds in mainstream cigarette smoke. This study used
mass spectrometry to identify and quantify benzene and certain
other volatile compounds of interest in the mainstream smoke of
26 cigarette brands in the UK market, and smoke from hand rolled
cigarettes. The study concluded that smoking the majority of brands
examined could contribute significantly to the population's exposure
to benzene and the other volatile organic compounds considered.
Analyst, May 1998, Vol 123 (1095-1101).
— Roll-your-own smoke yields: theoretical
and practical aspects. This study showed that 57 per cent of RYO
cigarettes produced by smokers were above the (then current) maximum
tar yield of 15mg for manufactured cigarettes. Tobacco Control,
Summer 1998, Vol 7, No 2, p 168-175.
7. Ongoing research includes:
— Sidestream smoke yields. This work
is updating the methodology for determining named chemicals in
sidestream cigarette smoke. The changes in the design of the smoking
machines used to test tar, nicotine and CO has necessitated this
work, since the equipment used to capture the sidestream smoke
has had to be modified.
— Fate of nicotine. This work will
determine the amount of nicotine in a cigarette and account for
where it goes when burnt, be it into mainstream smoke, sidestream
smoke or retained by the filter, and to ascertain, if possible,
how much nicotine is in the particulate phase and vapour phase.
— Intense smoking parameters. This
work will compare the yields of tar, nicotine and carbon monoxide
obtained after smoking cigarettes on a machine using the current
FTC smoking parameters and those in use in British Columbia and
Massachussetts, where by varying puff volume, duration and interval
the cigarettes are smoked more intensively.
3. NICOTINE ADDICTION
8. The Committee was interested in the addictiveness
of nicotine. The Department would wish to supplement its oral
evidence with the following comments. These are of a fairly technical
nature, but can be summarized in the statement that nicotine is
a highly addictive drug, and is generally recognized as such by
scientists.
9. The current scientific view is that nicotine,
delivered through tobacco smoke, should be regarded as an addictive
drug. This is by reference to two widely-recognised definitions
of criteria for substance abuse: DSM-IV and ICD 10. The definitions
include the following criteria: a strong desire to take the drug;
difficulty in controlling use; higher priority given to drug use
than other activities and obligations; continued use despite harmful
consequences; and withdrawal symptoms. It is known that 40 per
cent of post-laryngectomy patients will continue to attempt to
smoke and 40 per cent of post-myocardial infarct (heart attack)
patients relapse to smoking whilst still in hospital. Tolerance
to nicotine exposure develops within a few hours in humans (smokers
and non-smokers) and animals.
10. An important publication which discussed
nicotine as a drug of addiction was the US Surgeon General's report
on Nicotine Addiction, 1988. The concept of nicotine as a drug
prompted moves in the US to regulate nicotine by the Food and
Drug Administration (FDA), an issue which is currently being challenged
by the industry. This whole area will be addressed fully in the
forthcoming Royal College of Physicians' new report "Nicotine
Addiction in Britain"(expected February 2000).
11. Evidence from the physical and pharmacological
effects of nicotine and the nicotine receptors in the brain has
increased understanding of the addictive process. Minute doses
of nicotine are observed to produce "burst firing" of
neuro-electrical activity within seconds, which is efficient in
mediating release of dopamine. Nicotine acetyl choline receptors
in the brain were mapped in 1980 and are situated in the mesolimbic
system in the ventral tegmental area of the nucleus accumbens.
Action on these receptors recruits dopamine and glutamatergic
neurotransmission into the dependence process. Stimulation of
the mesolimbic dopamine neurones is thought to play a central
role in development of addiction to nicotine and other drugs of
abuse.
12. Nicotine is a potent psychopharmacologically
active compound which produces mood changes in humans and serves
as a reinforcer in animals and humans. Animals allowed to self
administer nicotine exhibit withdrawal symptoms when the supply
is interrupted. These symptoms, which can also be precipitated
by nicotine antagonist administration, are cured by nicotine.
A ranking of addiction has been produced by Henningfield et
al (1995)1 which puts nicotine in prime position above heroin,
cocaine, alcohol and caffeine in terms of its dependence among
users.
13. It is important to appreciate that the
route of administration is critical to the addictive process.
The inhalation route, ie nicotine delivered by the cigarette,
provides high doses at a rapid rate that produce and sustain dependence.2
This contrasts with the oral and skin absorption routes, used
in nicotine dependence treatment products, which do not achieve
a high peak blood level of nicotine and are more slowly absorbed.
There is no evidence of abuse of these treatment products although
they assist in controlling nicotine withdrawal symptoms.
14. Another component to the use of tobacco
includes psycho-social patterns of behaviour which have to be
addressed by a smoker when attempting to quit. Cigarette smoking
also provides a number of sensory cues to the smoker, which can
be thought of as secondary reinforcers, and which predict the
reward or primary reinforcer (nicotine effect). These sensory
cues play a part in smoking behaviour.
REFERENCES
1. Henningfield JE, Shuh LM, Heishman.(1995).
Pharmacological determinants of cigarette smoking in: PBS Clarke,
M.Quik, FX Adlkofer and K Thurau (Eds). Effects of Nicotine on
Biological Systems II, Internation Symposium on Nicotine Advances
in Pharmacological Sciences (Basel, Birkhauser Verlag) p 254.
2. Dr Louis Harris, Evidence to the Food
and Drug Administration (FDA) on 3.8.94 on behalf of the College
on Problems of Drug Dependence and the American Society of Pharmacology
and Experimental Therapeutics.
4. THE BIOLOGICAL
SIGNIFICANCE OF
TOBACCO SPECIFIC
N-NITROSAMINES
15. Tobacco itself contains more than 2,000
chemical compounds including 30 carcinogens and tobacco smoke
has more than 4,000 constituents, including about 40 carcinogens.1,2
Nitrosamines as a group are found in tobacco and in tobacco smoke
and it has been known since the work of Magee and Barnes3 in 1956
that N-nitrodimethylamine is a powerful carcinogen in the rat.
Since that time the carcinogenic activity of over 200 nitrosamines
have been established in more than 30 species of animal.
Types of N-nitrosamines
16. During the processing of tobacco and
especially during tobacco smoking, three types of N-nitrosamines
are formed. They are:
1. The volatile nitrosamines.
2. The non-volatile nitrosamines.
3. The tobacco specific nitrosamines (TSNA).
17. The latter group (TSNA) are created
during the curing and smoking of tobacco and are formed by chemical
reactions with other constituents of tobacco including nicotine.
Two of the nitrosamines formed in this way have been shown to
produce cancer in animals (lung, oesophagus, trachea and nasal
cavity). Furthermore, one of these is a major organ specific to
the lung. The long term experimental finding has now been married
with the epidemiology of smoking and lung cancer and observations
on the changing smoking patterns of consumers of low yield filter
cigarettes. It is now known that the pathological type of malignant
tumour has changed over the last two decades. It is also known
that most smokers of lower tar/nicotine cigarettes inhale more
deeply than was necessary with the higher tar/nicotine cigarettes.
As a result of this intensity of smoking the deeper portion of
the lung may be exposed to higher amounts of all the carcinogenic
agents in smoke, including this "lung specific" nitrosamine.
With limited defence mechanisms in the periphery of the lung,
a different type of tumour results and an increase in adenocarcinoma
has been observed. This is the present working hypothesis and
highlights the potential role of nitrosamines.
18. Recent information would indicate that
one tobacco company is able to elute out these nitrosamines. Widespread
use of this technology would appear to offer a path to a "safer
cigarette" and the Department would wish to explore this.
It should be pointed out that use of this technology could result
in an alteration in the proportions of other carcinogens in the
tar component of cigarettes, and long term epidemiological studies
would be required to assess any health benefits accruing.
REFERENCES
1. Roberts, NL, Natural Tobacco Flavours.
Recent Adv Tob Sci, 14, 49, 1998.
2. Hoffman D and Hoffman I, Tobacco consumption
and lung cancer in "Lung Cancer. Advances in Basic and Clinical
Research". H.H. Hansen Ed, Kluwer Boston 1944, p 1-42.
3. Magee PN, Barnes JM (1956). The production
of malignant primary hepatic tumours in the rat by feeding dimethyl
nitrosamine. Br J Cancer, 10. P 114-122.
5. SOCIETAL COST
OF SMOKING
19. The Committee requested an estimate
of the social costs of smoking. What follows is a preliminary
view; if the Committee would find it helpful the Department could
do further work in this area.
20. In any estimate of this kind there are
decisions to be made on which costs to include. For example, should
one count among social cost only those costs which smokers do
not take into account because they do not meet them, such as fires
on other people's property caused by smoking? Or does social cost
also cover cost smokers impose on themselves such as premature
mortality? And does it cover only costs which can obviously be
expressed in money terms, such as fires, or also wider costs not
so amenable to conversion to money terms, such as premature deaths
from passive smoking.
21. Even in the grey areas some forms of
costing may be more acceptable than others. For example, if we
express the loss of life expectancy in money terms there is a
further decision to be made on what rate should be used.
22. The least controversial social cost
is arguably the value of property damage in fires caused by smoking.
Home Office has an estimate of the cost of property damage in
fires (other than commercial), and an estimate of the proportion
caused by smoking. By combining these figures, an estimate emerges
of £176 million a year.
23. The effects of passive smoking fall
into the same uncontroversial category. There is an estimate of
the cost of treating the effects of passive smoking in children
of £410 million a year.
24. Since taxation is not related to an
individual's use of health services, any extra cost smokers impose
on the NHS are often counted as social costs of smoking. There
are various estimates here ranging between £1.4 and £1.7
billion per annum in England.
25. There are various possible costs related
to the working environment. Since employees are not normally paid
less because they smoke, any lower productivity becomes a social
cost, not a private cost born by smokers. There is evidence that
smokers take longer breaks during work. Estimates of the cost
are wrapped up "total productivity losses" and may not
be on any great scale.
26. There are estimates of additional invalidity
benefit due to smoking related illness, amounting to some £330
million a year.
27. To sum up, the current evidence on the
social cost of smoking is patchy and would need to be firmed up.
The following table presents our preliminary views. Please note
that no estimate has been given for the cost of treating passive
smoking in adults. Nor has any monetary value been given for premature
deaths suffered by smokers. Any such value would probably be offset
in part by savings on, for example state pension payments.
SELECTED SOCIAL COSTS OF SMOKING
|
| £m pa
|
|
| — Fire damage to property (dwellings)
| 180 |
| — Costs of treating disease caused by passive smoking (children)
| 410 |
| — NHS costs of treating smoking related disease (current smokers)
| 1,400-1,700 |
| — Invalidity benfit (smoking related disease)
| 330 |
| Total | 2,320-2,350
|
|
6 LEGAL STATUS
OF THE
CONTROL MECHANISM
FOR TOBACCO
AND ITS
REGULATION
28. The following sets out the legal regulation and control
of tobacco products that currently exists under English and Community
law. There is a distinction to be made between tobacco products
and other tobacco-related products.
Tobacco as a consumer product
29. Tobacco is excluded from the scope of Part II of
the Consumer Protection Act 1987 (CPA), by virtue of section 10(7),
which defines consumer goods as:
"any goods which are ordinarily intended for private
use or consumption, not being:
30. Tobacco is defined under the Act[1]
as "any tobacco product within the meaning of section 1 (1)
of the Tobacco Products Duty Act 1979 and any article or substance
containing tobacco and intended for oral or nasal use. "This
means that cigarettes, cigars, hand-rolling tobacco, other smoking
tobacco and chewing tobacco, which are manufactured wholly or
partly from tobacco, or any substance used as a substitute for
tobacco, are excluded from the consumer safety provisions in the
CPA.
31. The CPA also defines "food" as "not
including tobacco but, subject to that, has the same meaning as
in the [Food Safety Act 1990]".
32. The Tobacco for Oral Use (Safety) Regulations 1992
prohibit the supply of tobacco for oral use.
Tobacco as a Medicinal Product
33. Tobacco is not defined as a controlled drug within
the meaning of the Misuse of Drugs Act 1979.
34. The Medical Devices Agency would have powers to control
tobacco related products which can be termed as medical devices
under the Medical Devices Regulation 1994,[2]
such as nicotine "patches", but not the tobacco product
itself. The manufacturer has a duty to comply with certain obligations
under the Regulations.
Tobacco as a Food Product
35. Tobacco does not fall within the definition of "food"
in the Food Safety Act 1990, and therefore is not covered by the
food health and safety provisions in that Act. The only possible
tobacco product which could be consumed and fall within the definition
of food would be oral tobacco, and this is prohibited from being
supplied under the Tobacco for Oral Use (Safety) Regulations 1992.
Restrictions on Tar and Nicotine
36. The Cigarettes (Maximum Tar Yield) (Safety) Regulations,[3]
set out maximum tar yields for cigarettes. These Regulations implement
Council Directive 90/239/EEC[4]
on the maximum tar yields for cigarettes. There is currently a
draft proposal for a new European Parliament and Council Directive
on tar yields, nicotine contents and labelling. Once adopted,
this European Parliament and Council proposal will afford Member
States a discretion as to how to implement the Directive in domestic
law.
Restrictions on Advertising and Packaging of Tobacco Products
37. Under the Tobacco Products Labelling (Safety) Regulations
1991,[5] producers are
required to ensure that tobacco products carry health warnings.
The Secretary of State has power to take samples and to test cigarettes
for compliance with the prescribed tar yields and health warnings.
December 1999
1
Section 19(1). Back
2
Medical Devices Regulations 1994 SI No 3017. Back
3
SI 1992 No 2783. Back
4
OJ 1990 L137/36. Back
5
SI 1991 No 1530, as amended by the Tobacco Products Labelling
(Safety) Regulations 1993, SI 1993 No 1947. Back
| 
