[ Editorials ]
In that series, it was not known whether the decedents
Smoking and Emphysema
Looking Beyond the Cigarette
David M. Mannino, MD, FCCP
Lexington, KY
The relation between cigarette smoking and the
development of emphysema and COPD has been well
documented.1,2 Although not all smokers develop disease,
among long-term smokers nearly 50% will have
evidence of obstruction on spirometry.3 Other forms of
smoke inhalation, such as exposure to biomass smoke
from cooking or heating, are also linked to the develop-
ment of COPD.4,5 Although there are several important
differences between these exposures, a key one is intent:
Cigarette smokers are intentionally exposing themselves
to high levels of particulate pollution, whereas those
exposed to biomass smoke are not doing this intentionally.
Other agents of abuse are also inhaled, some when they
are burned, such as crack cocaine or marijuana,6,7 and
others without burning, such as cocaine, inhalants, and
some narcotics.6 The report by Walker et al8 in this issue
of CHEST (see page 1156) is a case series of heroin
smokers who developed early onset emphysema. This
newly described phenomenon may offer insights into
the development of COPD and emphysema in cigarette
smokers.
What proportion of heroin users develops emphysema?
There is no good estimate for this, although a recent case
series of 55 deaths among heroin or methadone users
found 38% with emphysema on postmortem CT scan.9
AFFILIATIONS: From the Department of Preventive Medicine and
Environmental Health, University of Kentucky College of Public
Health.
CONFLICT OF INTEREST: D. M. M. has served as a consultant for
Boehringer-Ingelheim GmbH, GlaxoSmithKline, AstraZeneca,
Novartis AG, Merck & Co, and Forest Pharmaceuticals, Inc and has
received research grants from GlaxoSmithKline; Novartis AG;
Boehringer-Ingelheim GmbH; Forest Pharmaceuticals, Inc; and Pfizer
Inc. He is also compensated by Up-to-Date, has served as an expert in
tobacco-related cases, and is on the board of the COPD Foundation.
CORRESPONDENCE TO: David M. Mannino, MD, FCCP, Department
of Preventive Medicine and Environmental Health, University of
Kentucky College of Public Health, 111 Washington Ave, Lexington,
KY 40536; e-mail: dmannino@uky.edu
© 2015 AMERICAN COLLEGE OF CHEST PHYSICIANS. Reproduction of
this article is prohibited without written permission from the American
College of Chest Physicians. See online for more details.
DOI: 10.1378/chest.15-1454
1126 Editorials
were smoking narcotics nor was the smoking history
described, although the emphysema prevalence exceeds
that which would be expected in the general population.
How might narcotic use contribute to the development
of COPD and emphysema? There are several possible
explanations. One is that these diseases are related to
effects of narcotic use in general (rather than their mode
of administration). Supporting this are high levels of
C-reactive protein10 and other evidence of immune
stimulation in opiate-dependent people.11 However, data
from a study of national surveys in the United States do
not show a relation between heroin use and either chronic
bronchitis or asthma (although radiographic emphysema
was not specifically evaluated in that study).12
Another possible explanation is that the heroin being
used is contaminated with other agents. This phenom-
enon has been well documented; contaminants or other
pharmacologic agents such as talc6 or clenbuterol have
been cited.13 Many of these agents can damage either
the lungs per se or the pulmonary vasculature.14
The most likely explanation, however, relates to how the
heroin is being smoked by the user. Smokers of heroin
and other illicit substances typically take a deep inhala-
tion, combined with a Valsalva maneuver to enhance
absorption of the drug into the body.14 This has been
described previously in heroin users15 and users of other
smoked substances.6,16 In addition, these agents often
burn at a very high temperature, with the potential to
cause damage deep within the lung.14
The development of early onset emphysema in heroin
users is clearly important in its own right, but may also
inform the development of emphysema in nonopiate
users. For example, the depth of inhalation, dynamic
hyperinflation, and barotrauma may be important
factors in some patients who develop emphysema
related to cigarette smoking or other factors. Physicians
should be aware of this problem, and the general and
drug-using public must be educated about the dangers
associated with the inhalation of these and other burned
substances.
References
1. Ford ES, Croft JB, Mannino DM, Wheaton AG, Zhang X, Giles WH.
COPD surveillance–United States, 1999-2011. Chest. 2013;144(1):
284-305.
[ 148#5 CHEST NOVEMBER 2015 ]
 2. Ford ES, Mannino DM, Wheaton AG, Giles WH, Presley-Cantrell L,
Croft JB. Trends in the prevalence of obstructive and restrictive lung
function among adults in the United States: fi ndings from the
National Health and Nutrition Examination surveys from
1988-1994 to 2007-2010. Chest. 2013;143(5):1395-1406.
3. Lundbäck B, Lindberg A, Lindström M, et al; Obstructive Lung
Disease in Northern Sweden Studies. Not 15 but 50% of smokers
develop COPD?--Report from the Obstructive Lung Disease in
Northern Sweden Studies. Respir Med. 2003;97(2):115-122.
4. Kurmi OP, Semple S, Simkhada P, Smith WC, Ayres JG. COPD and
chronic bronchitis risk of indoor air pollution from solid fuel: a
systematic review and meta-analysis. Thorax. 2010;65(3):221-228.
5. Lamprecht B, McBurnie MA, Vollmer WM, et al; BOLD Collaborative
Research Group. COPD in never smokers: results from the
population-based burden of obstructive lung disease study. Chest.
2011;139(4):752-763.
6. Mégarbane B, Chevillard L. The large spectrum of pulmonary
complications following illicit drug use: features and mechanisms.
Chem Biol Interact. 2013;206(3):444-451.
7. Tashtoush B, Gonzalez-Ibarra F, Memarpour R, Hadeh A, Smolley L.
Vanishing lung syndrome in a patient with HIV infection and heavy
marijuana use. Case Rep Pulmonol. 2014; 2014:285208
8. Walker PP, Thwaite E, Amin S, Curtis JM, Calverley PMA. The
association between heroin inhalation and early onset emphysema.
Chest. 2015;148(5):1156-1163.
9. Winklhofer S, Surer E, Ampanozi G, et al. Post-mortem whole body
computed tomography of opioid (heroin and methadone) fatalities:
frequent findings and comparison to autopsy. Eur Radiol. 2014;
24(6):1276-1282.
10. Reece AS. High-sensitivity CRP in opiate addiction: relative and
age-dependent elevations. Cardiovasc Toxicol. 2012;12(2):149-157.
11. Reece AS. Chronic immune stimulation as a contributing cause of
chronic disease in opiate addiction including multi-system ageing.
Med Hypotheses. 2010;75(6):613-619.
12. Han B, Gfroerer JC, Colliver JD. Associations between duration of
illicit drug use and health conditions: results from the 2005-2007
national surveys on drug use and health. Ann Epidemiol. 2010;
20(4):289-297.
13. Wingert WE, Mundy LA, Nelson L, Wong SC, Curtis J. Detection
of clenbuterol in heroin users in twelve postmortem cases at the
Philadelphia medical examiner’s office. J Anal Toxicol. 2008;
32(7):522-528.
14. Milroy CM, Parai JL. The histopathology of drugs of abuse.
Histopathology. 2011;59(4):579-593.
15. Prowse SJ, Lima T, Irion KL, Burhan H, Hochhegger B, Marchiori E.
Valsalva manoeuvre effect on distribution of lung damage in heroin
inhalation. Br J Radiol. 2011;84(1006):e200-e201.
16. Shyamsunder AK, Gyaw SM. Pneumomediastinum: the Valsalva
crunch. Md Med J. 1999;48(6):299-302.
The Weighty Issue of
Obesity Management in
Sleep Apnea
Sanjay R. Patel, MD
Boston, MA
Reena Mehra, MD, FCCP
Cleveland, OH
The interrelationships between OSA and obesity are
complex in large part because of the multidirectional
nature of not only the association between these two
factors, but also their relationships with undesirable
journal.publications.chestnet.org
cardiovascular health outcomes. Indisputably, obesity
serves as a risk factor for OSA not only because of its
direct mechanical effects (ie, disadvantageously affecting
upper airways critical closing pressure), but also
potentially via pathophysiologic pathways involving a
reduction in lung volume resulting in a loss of caudal
traction of the upper airways and upper airways neuro-
modulatory effects of adipokines.1
The importance of obesity in OSA from a population
health level cannot be underestimated. Data from the
Wisconsin Sleep Cohort suggest that more than
one-half of cases of moderate to severe OSA are attribut-
able to excess weight.2 Although there is a widespread
belief that by improving sleep quality and reducing
fatigue OSA treatment can facilitate weight loss, data
from randomized controlled trials have established
that OSA therapy with CPAP does not produce weight
loss and actually leads to modest weight gain.3,4 Thus,
to achieve weight loss in overweight or obese patients
with OSA, adjunctive treatments specifically focused on
weight are necessary.
A number of randomized trials have evaluated the
impact of behavioral weight-loss interventions on OSA
severity. However, there have been limitations in this
literature, including such caveats as a focus on very low
calorie diets that are extremely intensive and not readily
available to most patients5,6 or studying patient popula-
tions incidentally found to have OSA who are not
necessarily representative of clinical OSA populations
in terms of both severity of OSA-related symptoms
and motivations to treat apnea.7 The study by Ng et al8
reported in this issue of CHEST (see page 1193)
represents one of the first trials to evaluate a long-term
lifestyle intervention in a population presenting for
treatment of OSA.
AFFILIATIONS: From Brigham and Women’s Hospital (Dr Patel),
Harvard Medical School; and the Cleveland Clinic (Dr Mehra).
CONFLICT OF INTEREST: S. R. P. has received honoraria from the
American Academy of Sleep Medicine, the American College of
Physicians, and Elsevier Publishing; positive airway pressure
machines and equipment from Philips Respironics; and grant
funding from the ResMed Foundation, the American Sleep
Medicine Foundation, and the National Institutes of Health.
R. M. has received honoraria from the American Academy of
Sleep Medicine, positive airway pressure machines and equipment
for research from Philips Respironics, and funding from the
National Institutes of Health.
CORRESPONDENCE TO: Reena Mehra, MD, Cleveland Clinic,
9500 Euclid Ave, Cleveland, OH 44195; e-mail: mehrar@ccf.org
© 2015 AMERICAN COLLEGE OF CHEST PHYSICIANS. Reproduction of
this article is prohibited without written permission from the American
College of Chest Physicians. See online for more details.
DOI: 10.1378/chest.15-1010
1127