30 Sum

20

Putt Putt

Volume (liters)
v
c
t

 

Puff Putt
1 id i Lt 1 jt i 1
10 20 30 40 50 60

Seconds

FIGURE 3.—Pattern of inhalation of cigarette smoke mixed

with air, in two smokers
SOURCE: Modified from Tobin et al. (1982b).

al. 1980a), 450 to 485 ml (Guillerm and Radziszewski 1978), 389 to
1,136 ml (Adams et al. 1983), 750 to 2,000 ml (Rawbone et al. 1978),
and 170 to 1,970 ml (Tobin et al. 1982b). A major factor in the
discrepancies between these studies is probably the inaccuracies
inherent in some of the methods employed in the measurements, as
discussed by Tobin and Sackner (1982). When inhalation volumes are
standardized for body size by relating them to vital capacity, marked
interindividual variation is still observed (Figure 3), with inhalation-
al volumes ranging from 9 to 47 percent of the vital capacity and a
group mean value of 20 percent (Tobin et al. 1982b). Smokers show
considerable variation in inhaled volumes while smoking a single
cigarette. The volume of inhalation bears no relationship to cigarette
consumption in terms of pack-years (Tobin et al. 1982b). Similarly,
duration of inhalation shows considerable variation between sub-
jects, with mean individual values ranging from 1.7 to 7.3 seconds
(Adams et al. 1983; Tobin et al. 1982b). Repeat measurements at
intervals of up to 10 months apart indicate that individual subjects
tend to maintain a fairly constant inhalation volume, duration of
inhalation, and associated breathhold time (Tobin et al. 1982b;
Adams et al. 1983).

351
The pattern of cigarette smoking shows a wide degree of intersub-
ject variability, including differences in the number of puffs, puff
volume, holding pause in the mouth, exhalation of smoke from the
mouth before inhalation, partitioning of airflow between the nose
and mouth, and volume and duration of inhalation. Given this
degree of variation, it is not surprising that smokers might show
wide differences in their individual susceptibilities to lung injury. In
a study relating inhalation volume—standardized for vital capaci-
ty—to the time-volume and flow-volume components of a forced vital
capacity maneuver, no significant correlation was observed (Tobin et
al. 1982b). Although this lack of a relationship might be interpreted
as indicating that the pattern of smoking is unimportant in the
development of lung disease, it may also reflect the fact that
pulmonary function was normal or near normal in the majority of
subjects and that the study was of a cross-sectional design.

Use of Additives in Low Tar and Nicotine Cigarettes

The nominal tar and nicotine yield of cigarettes has continually
decreased since the time of the initial reports linking smoking with
lung cancer (USDHHS 1981). In 1954, the average tar yield per
cigarette was 38 mg, and in 1980 it was less than 14 mg. Initially, tar
reduction was achieved by decreasing the cigarette tobacco content
or removing tar by smoke filtration, both of which probably resulted
in a lower smoke exposure. Since 1971, the reduction in tar yield has
exceeded the relative reduction in the weight of tobacco per
cigarette; this difference has increased since 1975 (USDHHS 1981).
Manufacturing technology has progressed beyond simple reduction
in tobacco content: the yield and composition of smoke can be
modified by genetic modification of the tobacco leaf (Tso 1972a),
changes in its cultivation and processing (Tso 1972b), changes in the
porosity of cigarette paper, and alterations in filter design (Kozlow-
ski et al. 1980b).

When initially introduced, lower yield cigarettes lacked palatabili-
ty and acceptability. Advertisements for the current low tar and
nicotine cigarettes emphasize their flavor, presumably achieved by
the use of additives in the processing of the tobacco. Additives
employed may include artificial tobacco substitutes (Freedman and
Fletcher 1976), flavor extracts of tobacco and other plants, exogenous
enzymes, powdered cocoa (Gori 1977), and other synthetic flavoring
substances. Perhaps more additives are being used in the new lower
tar and nicotine cigarettes than in the older brands, and new agents
may also be in use. Some of the substances, such as powdered cocoa,
have been shown to further increase the carcinogenicity of tar (Gori
1977), and others may result in increased or new and different
health risks. The pyrolytic products of these additive agents may

352
produce novel toxic constituents. A characterization of the chemical
composition and adverse biologic potential of these additives is
urgently required, but is currently impossible because cigarette
companies are not required to reveal what additives they employ in
the manufacture of tobacco (USDHHS 1981). No government agency
is empowered with supervisory authority in the manufacture of
tobacco products. With this lack of basic information and the usually
prolonged latent period before manifestation of the adverse effects of
smoking, it is likely that a long time period will elapse before we
know the hazards of the new cigarettes in current use.

Research Recommendations

1. Longitudinal epidemiologic studies are needed to determine
the risk for pulmonary symptoms and dysfunction in smokers
of cigarettes with the low tar and nicotine yields found in
currently popular brands.

2. Further research is needed to determine the relative potency of
high and low tar and nicotine cigarettes in inducing elastase
release and producing functional inhibition of ai-antitrypsin
activity.

3. Development of an animal model of cigarette-smoke-induced
emphysema would be advantageous in determining the relative
risk of lung injury of cigarettes of different composition.

4. More information is required on the smoking behavior of
smokers who have voluntarily switched from high to low tar
and nicotine cigarettes.

5. The role of cigarette tar, as opposed to nicotine content, in
determining smoking behavior needs to be defined.

6. Standard research cigarettes of varying tar and nicotine
contents that are palatable and acceptable to smokers need to
be developed.

7.The role of variation in smoking behavior in determining
susceptibility to lung injury needs to be defined. Studies are
required to determine the effect of smoking patterns on the
distribution and penetration of the smoke aerosol into the lung.

8. More information is needed on the composition and adverse
biologic effects of flavor additives in cigarettes and their
pyrolytic products.

Summary and Conclusions

1. The recommendation for those who cannot quit to switch to
smoking cigarette brands with low tar and nicotine yields, as
determined by a smoking-machine, is based on the assumption
that this switch will result in a reduction in the exposure of the

353
354

lung to these toxic substances. The design of the cigarette has
markedly changed in recent years, and this may have resulted
in machine-measured tar and nicotine yields that do not reflect
the real dose to the smoker.

.Smoking-machines that take into account compensatory

changes in smoking behavior are needed. The assays could
provide both an average and a range of tar and nicotine yields
produced by different individual patterns of smoking.

._ Although a reduction in cigarette tar content appears to reduce

the risk of cough and mucus hypersecretion, the risk of
shortness of breath and airflow obstruction may not be
reduced. Evidence is unavailable on the relative risks of
developing COLD consequent to smoking cigarettes with the
very low tar and nicotine yields of current and recently
marketed brands.

_ Smokers who switch from higher to lower yield cigarettes show

compensatory changes in smoking behavior: the number of
puffs per cigarette is variably increased and puff volume is
almost universally increased, although the number of ciga-
rettes smoked per day and inhalation volume are generally
unchanged. Full compensation of dose for cigarettes with lower
yields is generally not achieved.

Nicotine has long been regarded as the primary reinforcer of

cigarette smoking, but tar content may also be important in
determining smoking behavior.

. Depth and duration of inhalation are among the most impor-

tant factors in determining the relative concentration of smoke
constituents that reach the lung. Considerable interindividual
variation exists between smokers with respect to the volume
and duration of inhalation. This variation is likely to be an
important factor in determining the varying susceptibility of
smokers to the development of lung disease.

Production of low tar and nicotine cigarettes has progressed

beyond simple reduction in tobacco content. Additives such as
artificial tobacco substitutes and flavoring extracts have been
used. The identity, chemical composition, and adverse biologi-
cal potential of these additives are unknown at present.
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360
CHAPTER 7. PASSIVE SMOKING

361

480-144 0 - 85 - 13
CONTENTS

 

Introduction

 

Differences in Composition of Sidestream Smoke and
Mainstream Smoke

 

Measurement of Exposure

 

Acute Physiologic Response of the Airway to Smoke in
the Environment

 

Symptomatic Responses to Chronic Passive Cigarette
Smoke Exposure in Healthy Subjects

 

Respiratory Infections in Children of Smoking Parents

 

Pulmonary Function in Children of Smoking Parents

 

Pulmonary Function in Adults Exposed to Involuntary
Cigarette Smoke

 

The Effect of Passive Smoke Exposure on People With
Allergies, Asthma, and COLD

 

Summary and Conclusions

 

References

363
Introduction

This chapter explores recent data that relate involuntary cigarette
smoke exposure to the occurrence of physiologic changes, symptoms,
and diseases in nonsmoking adults and children. Health effects
related to fetal exposure in utero, a subject that has been extensively
studied, are not discussed, although instances where such exposure
may relate to potential development are pointed out. The interested
reader is referred to several excellent recent reviews for a more
complete treatment of this issue (USDHEW 1979; USDHHS 1980;
Abel 1980; Weinberger and Weiss 1981).

Differences in Composition of Sidestream Smoke and
Mainstream Smoke

Involuntary (passive) smoking is defined as the exposure of
nonsmokers to tobacco combustion products from the smoking of
others. Analysis of the health effects of passive smoking requires not
only some knowledge of the constituents of tobacco smoke, but also
some quantitation of tobacco smoke exposure. Tobacco smoke in the
environment is derived from two sources: mainstream smoke and
sidestream smoke. Mainstream smoke emerges into the environment
after having first been drawn through the cigarette, which filters
some of the active constituents. The smoke is then filtered by the
smoker’s own lungs, and exhaled. Sidestream smoke arises from the
burning end of the cigarette and enters directly into the environ-
ment. Differences in the temperature of combustion, the degree of
filtration, and the amount of tobacco consumed all lead to marked
differences in the concentration of the constituents of mainstream
smoke and sidestream smoke (USDHEW 1979; Sterling et al. 1982;
Brunneman et al. 1978; National Academy of Sciences 1981;
Rylander et al. 1984). Many potentially toxic gas phase constituents
are present in higher concentration in sidestream smoke than in
mainstream smoke (Brunneman et al. 1978) (Table 1), and nearly 85
percent of the smoke in a room results from sidestream smoke.
Smaller amounts of smoke are contributed to the environment from
the nonburning end of the cigarette by diffusion through the paper
wrapping and by the smoke exhaled by the smoker. Therefore, both
active and passive smokers may be similarly exposed to sidestream
smoke. Mainstream smoke is inhaled directly into the lungs and is
diluted only by the volume of air breathed in by the smoker when he
or she inhales. Sidestream smoke is generally diluted in a considera-
bly larger volume of air. Thus, passive smokers are subjected to a
quantitatively smaller and qualitatively different smoke exposure
than active smokers. The quantification of the exposure of a passive
smoker to these sidestream smoke constituents is often difficult.
Factors such as the type and number of cigarettes burned, the size of

365
the room, the ventilation rate, and the smoke residence time are all
important variables in determining levels of exposure. Thus, no
single variable accurately characterizes exposure to smoke constitu-
ents.

Repace and Lowrey (1980, 1982, 1983) have shown that, to a
reasonable approximation, exposure to the particulate phase is
predicted by the ratio of the smoker density to the effective
ventilation rate of the area in which the smokers are located.

Measurement of Exposure

Levels of indoor byproducts of tobacco smoke, with measurements
made under realistic exposure conditions, are presented in Table 2.
Among the constituents that have been measured, nitrogen oxide,
carbon monoxide, nicotine and respirable particulates, nitrosamines,
and aldehydes have been shown to be significantly elevated indoors
as a result of cigarette smoking. Nitrogen oxide is rapidly oxidized to
nitrogen dioxide (NOz) in air, and reaches equilibrium with outdoor
levels of NOz, provided there are suitable air exchange rates and no
other indoor sources, such as a gas stove. The particulate concentra-
tion indoors clearly increases with increasing numbers of smokers,
although the background level is determined by the outdoor level.
The conclusions from the few studies that actually measure ventila-
tion rates during exposure suggest that under “normal” air circula-
tion conditions, carbon monoxide (CO) levels will be relatively low,
but still may exceed the ambient air quality standard of 9 ppm
(NIOSH 1971). However, even modest reductions in ventilation rates
can lead to CO accumulation.

A variety of measures have been utilized to quantify the nonsmok-
er’s exposure to tobacco smoke. No single measure has been
uniformly accepted as characterizing the level of smoke. Nicotine is
the most tobacco-specific of these measures, but it is relatively
complicated and expensive to measure and settles out of the air with
the particulate phase, making it a poor measure of gas phase
constituents. In addition, nicotine may rapidly deposit on surfaces
and subsequently evaporate into the environment (Rylander et al.
1984), making it a poor measure of acute smoke exposure levels.
Measurements of total particulate matter are a broader measure of
smoke exposure, particularly if the measurements are limited to
particles in the respirable range and to environments without other
major sources of respirable particles. The smoke particles also settle
out of the air and therefore may not reflect the levels of gas phase
constituents, and a wide variety of other dusts may contribute
particulates to the air, particularly in the occupational setting. A
number of authors have measured levels of CO. This measurement is
relatively simple and a measure of absorption (carboxyhemoglobin)

366
L9E

TABLE 1.—Ratio of selected constituents in sidestream smoke (SS) to mainstream smoke (MS)

 

 

Gas phase constituents MS SS/MS ratio Particulate phase constituents MS SS/MS ratio
Carbon dioxide 20-60 mg 8.1 Tar 1-40 mg 1.3
Carbon monoxide 10-20 mg 25 Water 14 mg 24
Methane 1.3 mg 3.1 Toluene 108 pg 5.6
Acetylene 27 wg 08 Phenol 20-150 pg 2.6
Ammonia 80 pg 73.0 Methylnaphthalene 2.2 ug 28
Hydrogen cyanide 430 pg 0.25 Pyrene 50-200 pg 3.6
Methylfuran 20 pe 3.4 Benzofa}pyrene 20-40 pg 3.4
Acetonitrile 120 pg 39 Aniline 360 pg 30
Pyridine 32 ug 10.0 Nicotine 1.0-2.5 mg 2.7
Dimethylnitrosamine 10-65 yg 52.0 2-Naphthylamine 2 ng 39

 

Adapted from U.S. Department of Health, Education, and Welfare (1979).
898

TABLE 2a.—Acrolein measured under realistic conditions

 

 

 

Levels
Type of Monitoring

Study premises Occupancy Ventilation conditions Mean Range
Badre et al. Cafes Varied Not given 100 mL samples 0.03-0.10 mg/m*
(1978) Room 18 smokers Not given 100 mL samples 0.185 mg/m*

Hospital lobby 12 to 30 smokers Not given 100 mL samples 0.02 mg/m*

2 train compartments 2 to 3 emokers Not given 100 mL samples 0.02-0.12 mg/m?

Car 3 smokers Natural, open 100 mL samples 0.03 mg/m*

2 smokers Natural, closed 100 mL samples 0.30 mg/m*

Fischer et al. Restaurant 50-80/470 m?® Mechanical 27 x 30 min samples 7 ppb
(1978) and Restaurant 60-100/440 m? Natural 29 x 30 min samples 8 ppb
Weber et al. Bar 30-40/50 m* Natural, open 28 x 30 min samples 10 ppb
(1979) Cafeteria 80-150/574 m? 11 changes/hr 24 x 30 min samples 6 ppb (5 ppb

nonsmoking section)

 
69€

TABLE 2b.—Aromatic hydrocarbons measured under realistic conditions

 

 

 

 

 

Levels Nonsmoking controls
Type of Monitoring
Study premises Occupancy Ventilation conditions Mean Range Mean Range
Benzene (mg/m*)
Badre et al. Cafes Varied Not given 100 mL samples 0.05-0.15
(1978) Room 18 smokers Not given 100 mL samples 0.109
Train compartments 2 to 3 smokers Not given 100 mL samples 0.02-0.10
Car 3 smokers Natural, open 100 mL samples 0.04
2 smokers Natural, closed 100 mL samples 0.15
Toulene (mg/m°) _
Cafes Varied Not given 100 mL samples 0.04~1.04
Room 18 smokers Not given 100 mL samples 0.215
Train compartments 2 to 3 smokers Not given 100 mL samples 1.87
Car 2 smokers Natural, closed 100 mL samples 0.50
Benzofa}pyrene (ng/m’)
Elliott and Rowe Arena 8,647-10,786 people Mechanical Not given TA
(1975) 12,000-12,844 people Mechanical Not given 99
13,000-14,277 people Mechanical Not given 21.7
Separate non- 0.69
activity days
Galuskinova Restaurant Not given Not given 20 days in summer 6.2
(1964)

18 days in the fall

28.2-144

 
OLE

TABLE 2b.—Continued

 

 

 

 

 

 

 

 

 

Levels Nonsmoking controls
Type of Monitoring
Study premises Occupancy Ventilation conditions Range Mean Range
Just et al. Coffee houses Not given Not given 6 hr continuous 0.25-10.1 4.0-9.3 (outdoors)
(1972)
Benzofelpyrene (ng/m*)
3.3-23.4 3.0-5.1 (outdoors)
Bei hi lene (ng/m*
5.9-10.5 6.9-13.8 (outdoors)
Perylene (ng/m?)
0.7-1.3 0.1-1.7 (outdoors)
Pyrene (ng/m’)
4.1-9.4 2.8-7.0 (outdoors)
Anthanthrene (ng/m‘)
05-19 0.5-1.8 (outdoors)
Coronene (ng/m’)
0.5-1.2 10-28
Phenols (1/m*)
TAALS
Benzofalpyrene (ng/m’)
Perry (1973) 14 public places Not given Not given Samples, 5 outdoor < 20-760 < 20-43

locations
TLE

TABLE 2c.—Carbon monoxide measured under realistic conditions

 

 

 

Levels (ppm) Nonsmoking controls (ppm)
Type of Monitoring
Study premises Occupancy Ventilation conditions Mean Range Mean Range
Badre et al. 6 cafes Varied Not given 20 min samples 2-23 (outdoors) 0-15
(1978) Room 18 smokers Not given 20 min samples 50 0 (outdoors)
Hospital lobby 12 to 30 smokers Not given 20 min samples 5
2 train 2 to 3 smokers Not given 20 min samples 45
compartments
Car 3 smokers Natural, open 20 min samples 14 0 (outdoors)
2 smokers Natural, closed 20 min samples 20 0 (outdoors)
Cano et al. Submarines 157 cigarettes Yes <40 ppm
(1970) 66 m’ per day
94-103 cigarettes Yes <40 ppm
per day
Chappell and 10 offices Not given Values not 17 x 23 min 25 + 10 1.54.5 25 + 10 15-45
Parker given samples (outdoors)
(1977) 15 restaurants Not given Values not 17 x 23 min 40+ 25 1.0-9.5 25+ 15 1.0-5.0
given samples (outdoors)
14 nightclubs Not given Values not 19 x 23 min 13.0 + 7.0 3.0-29.0 3.0 + 2.0 1.0-5.0
and taverns given samples (outdoors)
Tavern Not given Artificial 16 x 23 min 85
samples
None 2x 23 min 35 (peak)
samples
Offices 1440 ft? Natural, open 2-3 min samples 10.0 (peak)
30 min after 1.0
smoking

 
oLe

TABLE 2c.—Continued

 

 

 

Levels (ppm) Nonsmoking controls (ppm)
Type of Monitoring
Study premises Occupancy Ventilation conditions Mean Range Mean Range
Coburn et al. Rooms Not given Not given Not given 4.3-9.0
(1965) Nonsmokers’ rooms 2.2 + 0.98 0.44.5
Cuddeback Tavern 1 10-294 people 6 changes/hr 8 hr continuous 11.5 10-12 2 (outdoors)
et al. 2 hr after smoking ~l
(1976) Tavern 2 Not given 1-2 changes/hr 8 hr continuous 17 ~3-22 Values not given
2 hr after smoking ~12 Values not given
US. Dept. of 18 military 165-219 people Mechanical 6-7 hr continuous <25
Transportation planes
(1971 8 domestic 27-113 people Mechanical 1'/,-2", br <2
planes continuous
Elliott and Arena | 11,806 people Mechanical Not given 9.0 3.0 (nonactivity day)
Rowe Arena 2 2,000 people Natural Not given 25.0 3.0 (nonactivity day)
(1975¢ Nonsmoking 9.0
arena
Fischer et al. Restaurant 50-80/470 m? Mechanical 27 x 30 min 5.1 2.1-9.9 4.8 (outdoors)
(1978) and samples
Weber et al. Restaurant 60-100/440 m? Natural 29 x 30 min 2.6 1.4-3.4 1.5 (outdoors)
(1979) samples
Bar 30-40/50 m’ Natural, open 28 x 30 min 48 2.4-9.6 1.7 (outdoors)
samples
Cafeteria 80-150/574 m* 11 changes/hr 24 x 30 min 1.2 0.7-1.7 0.4 (outdoors)
Nonsmoking 0.5 0.3-0.8
room
Godin et al. Ferryboat Not given Not given 11 grab samples 18.4 + 87 3.0 + 2.4 (nonsmoking room)
(1972) Theater foyer Not given Not given Grab samples 34+ 08 1.4 + 0.8 (auditorium)

 
TABLE 2c.—Continued

 

 

Levels (ppm) Nonsmoking controls (ppm)
Type of Monitoring
Study premises Occupancy Ventilation conditions Mean Range Mean Range
Harke Offices ~72 m? 236 m*/hr 30 min samples <25-46
(1974a) Offices ~78 m? Natural 30 min samples <25-9.0
Harke and Car 2 smokers Natural Samples 42 (peak) (Nonsmoking runs)
Peters (4 cigs) 13.5 (peak)
(19745 Mechanical Samples 32 (peak) (Nonsmoking runs)
15.0 (peak)
Harmeen and Train 1-18 smokers Natural Not given 0-40
Effenberger
(1957
Perry 14 public Not given Not given One grab sample <10
1973) places
Portheine Rooms Not given Not given Not given 5-25
t197)8
Sebben et al. 9 nightclubs Not given Varied 77 x 1 min 13.4 65-419
(1977 samples
Outdoors 9.2 3.0-35.0
14 restauranta Not given Not given Spot checks 99 + 55 Values not given
45 restaurants Not given Not given Spot checks 82 4 22 7.1 + 1.7 (outdoors)
33 stores Not given Not given Spot checks 10.0 + 4.2 115 + 69 (outdoors)
3 hospital Not given Not given Spot checks 438 Values not given
lobbies

 

ELE
PLE

TABLE 2c.—Continued

 

 

Levels (ppm) Nonsmoking controls (ppm)
Type of Monitoring
Study premises Occupancy Ventilation conditions Mean Range Mean Range
Seiff Intercity bus Not given 15 changes/hr, 33 ppm
(1973) 23 cigarettes
burning
continuously
3 cigarettes 18 ppm
burning
continuously
Slavin and 2 conference Not given 8 changes/hr Continuous, 8 (peak) 1-2 (separate
Hertz rooms morning nonsmoking day)
(1975) 6 changes/hr Continuous, 10 (peak) 1-2 (separate
morning nonsmoking day)
Szadkowski 25 offices Not given Not given Continuous 2.78 + 1.42 259 + 2.23
et al. (separate nonsmoking
(1976) offices)

 

«Three cigarettes and one cigar smoked in 20 minutes.

>The Drager tube used is accurate only within + 25 percent.

©The MSA Monitaire Sampler used is accurate only within + 25 percent.

4 About 40 cigarettes/day were smoked.
* About 70 cigarettes/day were smoked.
Four filter cigarettes were smoked.
© No experimental deacription given.
wo
<1
on

TABLE 2d.—Nicotine measured under realistic conditions

 

 

 

Nonsmoking
Levels (ug/m?) controls
Type of Monitoring
Study premises Occupancy Ventilation conditions Mean Range Mean Range
Badre et al. 6 cafes Varied Not given 50 min sample 25-52
(1978) Room 18 smokers Not given 50 min sample 500
Hoapital lobby 12 to 30 smokers Not given 50 min sample 37
2 train compartments 2 to 3 smokers Not given 50 min sample 36-50
Car 3 smokers Natural, open 50 min sample
Natural, closed 50 min sample 1010
Cano et al. Submarines 157 cigarettes Yes 32 pg/m?
(1970) 66m‘ per day
94-103 cigarettes Yes 15-35 g/m?
per day
_Harmsen and Train Not given Natural, closed 30-45 min 07.-3.1
‘ Effenberger samples
(1967)
Hinds and First Train Not given Not given 2’, hr samples 49 Values not given
(1975) Bus Not given Not given 2 hr samples 6.3 Values not given
Bus waiting room Not given Not given 2, hr samples 1.0 Values not given
Airline waiting room Not given Not given 2%, hr samples 3.1 Values not given
Restaurant Not given Not given 2", hr samples 5.2 Values not given
Cocktail lounge Not given Not given 2, hr samples 10.3 Values not given
Student lounge Not given Not given 2‘, hr samples 28 Values not given
Weber and Fischer 44 offices Varied Varied 140 x 3 hr 0.9 + 19 13.8 (peak) Values not given
(1980 samples

 

* Background levels have been subtracted.

‘Control values (unoccupied rooms) have been subtracted.