Environmental Tobacco Smoke

Environmental tobacco smoke (ETS) is comprised of sidestream smoke (about
80% released from burning tobacco in between puffs), and
from the exhaled smoke (about 20% of the smoke). The smoke
that the smoker inhales is known as mainstream smoke. Other
minor contributors to ETS include the smoke that escapes during
puffing from the burning cone, and gaseous components
that diffuse through the cigarette paper. These components are
diluted by the ambient air and when inhaled, in particular by
nonsmokers, are referred to as “passive” or “involuntary” smoking.
ETS contains various toxic agents, including mutagens
and carcinogens, which, for some chemicals (e.g., nitrosamines,
4-aminobiphenyl, benzo[a]pyrene), have been measured at
higher concentrations than in mainstream smoke. Estimates
of ETS exposure, based on serum or urinary measurements of
cotinine, the metabolite of nicotine, suggest that involuntary
smokers absorb about 0.5% to 1% of the nicotine that active
smokers absorb, or smoke the equivalent of about one-half cigarette
a day. Studies of 4-aminobiphenyl-hemoglobin adduct
levels indicate that passive smokers have approximately 14% of
the concentration of active smokers. 46
Many scientific consensus committees have concluded
that exposure to ETS causes lung cancer in humans. Table 1.4
lists the RRs of lung cancer among nonsmoking women based
on a review of epidemiologic studies in various countries,
which have evaluated dose–response trends. 47–64 The risks increased
with amounts smoked by husbands, with about 30%
to 150% increases in RR experienced in general among those
women most heavily exposed. A weighted analysis of 37 published
epidemiological studies resulted in the conclusion that
there was an elevated risk of 24% (95% confidence interval
[CI], 13% to 36%) among nonsmoking wives of smoking husbands,
when compared with nonsmoking wives of nonsmoking
husbands. Workplace exposures to ETS are measured with
less precision than spousal exposures; however, some studies
have suggested that there is a dose–response relationship when
combining workplace and spousal sources of ETS. It has been
suggested that when using biological markers of nicotine exposure
in studies of ETS and lung cancer, about 5% of female
respondents, who were in fact smokers, may have reported
that they were nonsmokers. Correcting for this bias, however,
would result in an adjusted RR in nonsmoking women who
were living with smokers of about 1.15 to 1.20. The report of
the National Research Council concluded that about 20% of
lung cancers occurring in nonsmoking women and men, or
3000 cases per year, may be attributable to exposure to ETS;
in the context of lung cancer cases diagnosed each year in
smokers and nonsmokers, 2% to 3% may be attributable to
ETS. 65,66
Air Pollution Pollutants in the urban air other than from
tobacco have been investigated as potential causal agents in
the epidemic rise of lung cancer in industrialized nations. The
products of fossil fuel combustion, principally polycyclic hydrocarbons,
have been of particular concern. Other sources of
ambient air pollution have been motor vehicle and diesel engine
exhausts, power plants, and industrial and residential emissions.
The ratio of urban to rural age-adjusted lung cancer mortality
rates in many industrialized nations have varied between 1.1
and 2.0. It has been suggested that the net attributable risk effect
of protracted exposure to urban air pollutants in men with
average smoking habits would be 10 cases of lung cancer per
100,000 per year. In most countries, however, a major fraction
(i.e., 80% or greater) would be attributable to cigarette smoking,
and the independent association with urban residence, or
the “urban factor,” could not be assessed without controlling
for the confounding effect of differences in smoking practices,
or exposures to environmental tobacco smoke, between urban
and rural residents. In addition, the urban factor has yet to be
defined, but is undoubtedly a complex mixture of interacting
chemical compounds and elements that vary by geographic area
and over time. Exposure to combustion-source ambient air pollution
has been associated with declining pulmonary function,
increased rates of hospitalization for respiratory illnesses, and
increased rates of cardiopulmonary diseases mortality. 67–69
Evidence in support of the potential association of air
pollution with lung cancer may be provided by occupational
studies of workers exposed to combustion products from fos-
sil fuels. Workers exposed to emissions from retort coal gas
plants manifested smoking-adjusted RR of lung cancer that
was approximately twice that in unexposed workers. Roofers
exposed to coal tar fumes while working outdoors had an approximately
50% increase in lung cancer risk after 20 years of
exposure, and 150% increase after 40 years. 70,71
Benzo(a)pyrene has been used as a surrogate index of
ambient urban air exposure produced by fossil fuel combustion
and correlated with lung cancer mortality rates. However,
putative carcinogenic agents present in ambient urban air
may include inorganic particles or fibers (e.g., arsenic, asbestos,
chromium, nickel, uranium); radionuclides (e.g., 210 Pb,
212 Pb, 222 Ra); and organic gaseous and particulate combustion
products (e.g., dimethylnitrosamine, benzene, benzo[a]pyrene,
1,2-benzanthracene). In a longitudinal study by the ACS, age-,
occupational-, and smoking-standardized rates for lung cancer
were computed according to residence. Minimal differences in
mortality were observed between urban and rural residential
areas, or among cities categorized by indices of pollution. 72
The World Health Organization (WHO) IARC has declared
diesel engine exhaust a “probable carcinogen.” In studies of
railroad workers exposed to diesel exhaust, Garshick et al. described
a 40% increase in the smoking-adjusted RR of lung
cancer. 73,74
In a rural area in Yunan Province, China, an excess risk of
lung cancer among men and women was attributed to indoor
pollution because of burning soft, “smoky” coal in unvented
firepits inside the home. Replacing the firepits with stoves
vented with chimneys was reported to reduce lung cancer incidence
by about 40% to 45%. 75 In Shanghai, the elevated risk
of lung cancer was hypothesized to be a result of prolonged
exposure to oil vapors, particularly from rapeseed oil that was
used in high-temperature wok cooking. Condensates of the
volatile emissions from rapeseed and soybean oil have been
found to be mutagenic. In urban Shenyang in northeastern
China, indoor pollution from coal-burning heating devices
gave rise to an age-, education-, and tobacco smoking-adjusted
RR of 2.3 for lung cancer in the highest exposure group. 76–78
Indoor Radon Radon ( 222 Ra), with a half-life of 3.8 days,
is an inert, radioactive, colorless, and odorless gas at usual environmental
temperatures that can percolate through the earth’s
crust and accumulate in residential dwellings. At sufficiently
high concentrations, radon and its -particle–emitting decay
products, polonium-214 and polonium-218, have been shown
to cause lung cancer in cigarette smoking and nonsmoking uranium,
tin, and iron-ore miners. These observations have been
replicated by conducting experimental studies in rats. 79 Indoor
radon exposure accounts for about 50% to 80% of the total radiation
received on average in the United States. It has been estimated,
based on extrapolations from high-risk miner studies,
that indoor radon may cause between 6000 and 36,000 lung
cancer deaths per year in the United States. Joint exposures to
tobacco smoke and radon gas have been interpreted to yield
risks of lung cancer that were greater than linear and additive
and approximated multiplicative or log linear effects. 80–82
Case-control studies of lung cancer have been conducted
in various countries based on estimated lifetime exposures to
residential radon and tobacco smoke. Axelson et al. 83 noted
an increased risk of lung cancer among persons living in stone
compared to wood houses in Sweden. In a later study by
Pershagen et al.,84 it was concluded that the smoking-adjusted
risk of lung cancer increased in relation to the cumulative and
time-weighted exposure to radon. The RR was 1.3 (95% CI,
1.1 to 1.6) for average radon concentrations, over a period of
about 30 years, of 3.8 to 10.8 pCi per liter; for exposure in
excess of 10.8 pCi/L, the RR was 1.8 (95% CI, 1.1 to 2.9).
Moreover, there was evidence that the joint effect of radon
exposure and tobacco smoking was multiplicative rather than
additive. In a study conducted in New Jersey, the risk of lung
cancer was increased more than twofold among women living
in homes with radon levels exceeding 4 pCi/L. 85 However, in
a case-control study of women who were recently diagnosed
with lung cancer in China, no association was demonstrated
between increasing residential radon exposure and lung
cancer; 20% of the yearlong radon measurements exceeded
4 pCi/L, the level above which remedial action is recommended
in the United States. 86 Conclusions that were similar
to those from the study in China were presented based on a
study by Létourneau et al. 87 in Canada. Thus, although radon
and its -particle–emitting decay products are classified as a
human lung carcinogen, there has been uncertainty expressed
about whether or to what extent residential radon exposure
levels contributed to the lung cancer burden and how accurate
were predictions based on extrapolations from studies of underground
miners. Epidemiologic studies of indoor radon in
the United States must be interpreted with caution because of
limitations in estimating lifetime exposures based on current
exposure measurements. Exposure reconstruction is complicated
because persons reside in many homes throughout life,
and the time actually spent in each home may be only approximated.
Average prior residential exposure levels were generally
low, exceeding remedial action levels in 5% of United States
homes. Extrapolated RR estimates of less than 1.2, which was
associated with average residential exposures, would have been
potentially confounded by effects of active and environmental
tobacco smoke inhalation. Notwithstanding these caveats,
recent publications were supportive of risks of lung cancer associated
with residential radon exposure that were consistent
with extrapolations of risk using underground mining-based
models.