Journal of Cancer Therapy, 2012, 3, 364-371 Published Online September 2012 (
Effect of Impaired Lung Function on the Development and
Progression of Endobronchial Premalignant Lesions
Vijayvel Jayaprakash1,2,3, Gregory M. Loewen4, Martin C. Mahoney3,5, Samjot Dhillon5,
Sai Yendamuri6, D. Kyle Hogarth7, Enrique Machare-Delgado8, Ravi J. Menezes9,
Sandra M. Jacob5, Mary E. Reid1,3,5*
1Cancer Prevention and Population Sciences, Roswell Park Cancer Institute, Buffalo, USA; 2Department of Dentistry, Roswell Park
Cancer Institute, Buffalo, USA; 3Department of Social and Preventive Medicine, State University of New York at Buffalo, Buffalo,
USA; 4Pulmonary Oncology, Sacred Heart Medical Center, Spokane, USA; 5Department of Medicine, Roswell Park Cancer Institute,
Buffalo, USA; 6Department of Thoracic Surgery, Roswell Park Cancer Institute, Buffalo, USA; 7Section of Pulmonary and Critical
Care Medicine, University of Chicago, Chicago, USA; 8School of Medicine, State University of New York at Buffalo, Buffalo, USA;
9Department of Medical Imaging, University Health Network, Toronto, Canada.
Email: *
Received July 27th, 2012; revised August 29th, 2012; accepted September 11th, 2012
Background: Chronic obstructive pulmonary disease (COPD) and the presence of endobronchial premalignant lesions
(EPL) are individual risk factors for lung cancer (LC). However, effect of impaired lung function (ILF) on the natural
history of EPL has not been explored. Patients and Methods: This study included 217 high-risk participants from a
hospital-based LC surveillance cohort who underwent pulmonary function testing followed by bronchoscopy with en-
dobronchial biopsies. Baseline histopathology diagnoses included 91 cases (41.9%) with squamous metaplasia (SM), 25
(11.5%) with squamous dysplasia (SD), 1 (0.5%) with in-situ carcinoma and 5 (2.3%) with invasive LC. Follow-up
biopsies were obtained for 69 patients, and 16 (23.2%) patients demonstrated progression to a higher grade lesion. Re-
gression models were used to evaluate the relationship between ILF and EPL. All the models were adjusted for age,
gender and tobacco smoking. Results: Patients with FEV1% of <50% had 4.5 times greater risk of being diagnosed with
an EPL [95% confidence interval: 1.93 - 10.80] and 8-fold greater risk of SD, compared to patients with FEV1% 80.
COPD was associated with 2.7 and 4.8 times greater risk of SM and SD, respectively. The mean time to progression to
a higher-grade lesion was shorter in COPD patients compared to patients without COPD (27 versus 50 months, p =
0.02). Conclusion: Our results indicate that ILF may be a predictor of prevalence and progression of EPLs among pa-
tients at high risk of LC. Therefore, spirometry can be a complementary pre-screening tool for identifying patients with
EPL who need more intense LC surveillance.
Keywords: COPD; Lung Cancer; Premalignant Lesions; Dysplasia; Pulmonary Function Test; Spirometry
1. Introduction
Although the mortality rate due to lung cancer (LC) has
been steadily declining over the last decade, the overall
5-year survival rate has remained a dismal 15% [1]. This
poor survival rate can be attributed to the fact that most
patients have an advanced disease stage at diagnosis,
often limiting the management strategy to palliative op-
tions. While it is considered that early detection and
treatment can improve the long term survival rate of LC
patients [2], the efficacy and cost effectiveness of LC
screening in average or low risk populations is question-
able [3-5]. Therefore, selective targeted surveillance in
high risk patients is currently a more feasible way to de-
tect and treat the disease at the earliest stage.
Intra-epithelial lesions, like squamous metaplasia (SM),
squamous dysplasia (SD) and carcinoma-in-situ (CIS)
have been classified as precursors to invasive squamous
cell carcinoma of lung (SCC) [6-9]. Patients with these
endobronchial premalignant lesions (EPL) have been
shown to be at a much greater risk of developing a squa-
mous cell carcinoma of the lung. Targeted surveillance in
such high-risk subgroup will be a more efficient strategy
for early detection and chemoprevention. However, the
natural history of these EPLs and factors predicting the
progression of these lesions are not yet clear.
Chronic obstructive pulmonary disease (COPD) and
LC are both respiratory diseases that share similar risk
factors and disease mechanisms [10-12]. The “Global
*Corresponding author.
Copyright © 2012 SciRes. JCT
Effect of Impaired Lung Function on the Development and Progression of Endobronchial Premalignant Lesions 365
Initiative for Chronic Obstructive Lung Disease” (GOLD)
defines COPD as a disease with progressive airflow
limitation, which is not completely reversible [13]. Spi-
rometry is a widely available and inexpensive test for
evaluating the airflow limitation and lung function (LF).
It has been shown that patients with moderate to severe
COPD are at more than 4 fold increased risk of LC, with
a significant linear increase in risk with a greater degree
of airway obstruction [14-19]. However, the relationship
between impaired LF (ILF) and the risk of development
and progression of EPLs is less clear. Clarifying any
such association will be useful for defining a high risk
cohort in need of intense LC surveillance. This study was
conducted to examine the association between spiromet-
ric LF measurements and EPLs identified via broncho-
scopy aided biopsy.
2. Materials and Methods
2.1. Study Population
The LC Risk Assessment Center at Roswell Park Cancer
Institute (RPCI), Buffalo, NY, assesses and manages pa-
tients considered to be high risk by virtue of at least two
of the following risk factors: >20 pack-year history of
tobacco use, asbestos-related lung disease, diagnosed
chronic obstructive pulmonary disease with a forced ex-
piratory volume in per second (FEV1) < 70% of pre-
dicted, and/or prior aerodigestive or respiratory cancer
treated with curative intent with no evidence of disease
for at least 6 months prior to enrollment. As a component
of the evaluation, the patients undergo spirometry and a
computerized tomography (CT) of the chest, followed by
combined white light and autofluorescence bronchoscopy
with biopsies. Detailed demographic, histologic and cli-
nical history was collected on these patients. This study
was approved by the Institutional Review Board at RPCI.
The current analysis includes only high risk patients
who had at least one complete spirometric evaluation
within the 6 months preceding their baseline broncho-
scopic evaluation. Patients who had a history of previous
LC treated with a bi-lobectomy or pneumonectomy were
excluded. Patients with a previously diagnosed and un-
treated EPL (either SM, SD or CIS) were also excluded
from this analysis. The current analysis includes 217 pa-
tients who satisfied all the inclusion criteria. Among
these 217 persons, 69 completed a follow-up broncho-
scopy with biopsies and were evaluated for changes in
the lesions detected at the baseline bronchoscopy.
2.2. Clinical Exam and Data Collection
The patients underwent lung function tests using hand-
held spirometry based on American Thoracic Society
(ATS) guidelines [20]. The spirometric measurements
included FEV1 and forced vital capacity (FVC). FEV1/
FVC ratio was calculated using these values. The per-
centage of predicted value of FEV1 (FEV1%) and FVC
(FVC%) were calculated based on predicted equation of
Crapo et al. [21]. For patients who had more than one
spirometry performed within 6 months prior to baseline
examination, the spirometry performed closest to the date
of diagnosis was considered for this study. Broncho-
scopic examination was conducted using the light in-
duced fluorescence endoscopy (LIFE) device (Xillix
LIFE-Lung Fluorescence Endoscopy System, Xillix tech-
nologies Corp, Richmond, BC, Canada). Lesions identi-
fied under white light and/or fluorescent light were biop-
sied and were histopathologically graded as benign, SM,
SD (mild, moderate or severe), CIS and invasive LC
(SCC or adenocarcinoma of the lung). The follow-up
bronchoscopy was performed on a pre-specified schedule:
6 months to 1 year for patients with SD and 2 to 3 years
for patients with SM, unless there was any exacerbation
of symptoms warranting intermediary evaluation based
on clinical judgment.
3. Analysis
For analysis purposes, FEV1% was stratified into 3
groups: 80% (normal), 50% to <80% (mild/moderate
impairment) and <50% (severe impairment) and FEV1/
FVC was stratified as: 70% (normal), 50% to <70%
(mildly reduced) and <50% (moderately/severely re-
duced). The GOLD criterion was used to stratify patients
as mild, moderate and severe COPD [13]. According to
the GOLD criteria, a patient is diagnosed with mild
COPD if FEV1/FVC < 70% and FEV1 80%, moderate
COPD if FEV1/FVC < 70% and 50% FEV1 80% and
severe COPD if FEV1/FVC < 70% and FEV1 < 50%. The
association between ILF and the odds of detecting EPLs
was examined by calculating adjusted odds ratio (OR)
and 95% confidence intervals (CI) using unconditional
logistic regression. The risk estimates reported here were
adjusted for other significant risk factors like age at time
of spirometry, gender and pack-years of cigarettes
smoked. The highest histopathologic grade lesion for
each person determined the final diagnosis for analytic
purpose. For example, if a patient had both SM and
moderate SD, the final diagnosis for analytic purposes
was moderate SD. Due to the limited number of SDs
detected, all grades of SD (mild, moderate and severe)
were grouped together for this analysis. Similarly, CIS
and LC were also grouped together for analysis purposes.
For the follow-up analysis, any change to a higher grade
lesion on follow-up biopsy was considered as progress-
sion. The risk of progression for baseline EPLs was
evaluated using hazard ratios (HR) based upon Cox re-
gression models. Risk estimates were adjusted for other
Copyright © 2012 SciRes. JCT
Effect of Impaired Lung Function on the Development and Progression of Endobronchial Premalignant Lesions
risk factors like age at time of spirometry, gender and
pack-years of cigarettes smoked. The statistical package
SPSS version 15.0 (SPSS Inc., Chicago, Ill) was used to
conduct these analyses.
4. Results
The descriptive characteristics of the 353 patients in the
overall screening cohort and the 217 participants in-
cluded in this analysis are presented in Table 1. More
than two-thirds of the 217 patients were males and most
self-identified as Caucasian. About 93.1% of the study
participants were either former or current smokers and
41.9% reported a history of asbestos exposure. Based on
baseline biopsy, 91 patients (41.9%) were diagnosed with
SM, 12 (5.5%) with mild SD, 10 (4.6%) with moderate
SD, 3 (1.4%) with severe SD and 1 (0.5%) with CIS, 4
(1.8%) with SCC and 1 (0.5%) with adenocarcinoma.
Table 2 presents the risk estimates for the identifica-
tion of EPLs based on categorical measures of FEV1%,
FEV1/FVC values and COPD. The category of most se-
vere FEV1% impairment (<50% of predicted) was asso-
ciated with more than 4.5 times greater risk of detecting
EPLs, compared to FEV1% of 80%. Results were simi-
lar for categories of FEV1/FVC and when SM and SD
were individually examined. Significant trends in the risk
of EPLs were noted with increasing severity of COPD
overall and within categories of lesions. Similar analysis
was also performed for linear estimates of FEV1% and
FEV1/FVC (Figure 1). The results showed a trend for
increased risk of detection of EPLs associated with the
decreased LF measured by every liter decrease in FEV1
volume and every 10% decrease in the FEV1/FVC ratio.
The risk of detecting EPLs was also analyzed separately
for males and females (Table 3). A statistically signifi-
cant increase in risk associated with the highest category
of airflow limitation was observed in both genders. The
risk of detecting EPLs in patients with FEV1% < 50 was
3.8 times greater in males and 6.5 times greater in fe-
males, compared to patients with FEV1% > 80.
We analyzed the risk of progression from baseline
EPLs based on COPD status at baseline (Figure 2). A
total of 69 patients who completed both baseline and
follow-up bronchoscopy were included; follow-up bron-
choscopy was completed at a median follow-up interval
of 13 months (range: 5 to 73 months). The baseline de-
mographic characteristics of the 69 patients were com-
parable to the overall population of 217 patients (Table
1). In 16 of the 69 patients (23%) the baseline lesion
progressed to a higher grade, including 11 of 44 (25%)
patients with COPD and 5 of 25 (20%) patients without
COPD at baseline. The range of time to progression of
lesions on these patients was 7 to 73 months. Among
these 16 patients, 10 patients had their baseline SM pro-
gress (6 to mild SD and 4 to moderate SD), 2 patients
BenignMetaplasia Dysplasia
Lesion Type
Odds ratio
1.19 (1.01-1.35)
1.39 (1.13-1.58)
1.39 (1.12-1.59)
1.53 (1.08-1.76)
Measured FEV1—every one litre decrease
FEV1/FVC—every 10% decrease
Figure 1. Trend in the odds of detecting premalignant le-
sions based on linear measures of lung function.
Subjects with COPD
Subjects without COPD
+ Censored
Figure 2. Kaplan-Meier curve to evaluate the difference in
progression of baseline premalignant lesions based on
COPD status (GOLD criteria).
had their mild SD progress to moderate SD and one pa-
tient who had a moderate SD at baseline progressed to
severe SD. In 3 other patients who did not have any
baseline EPL, 2 were diagnosed with mild SD and 1 pa-
tient had moderate SD on follow bronchoscopy. The
hazard ratio for the risk of progression was calculated
based on a Cox regression model, adjusting for age,
gender and pack-years of smoking. The results show that
the patients with COPD had a non-statistically significant
2.5 times greater risk of their baseline lesion progressing
Copyright © 2012 SciRes. JCT
Effect of Impaired Lung Function on the Development and Progression of Endobronchial Premalignant Lesions
Copyright © 2012 SciRes. JCT
Table 1. Baseline demographic characteristics of all patients who were evaluated for the lung cancer surveillance study.
All screening patients
(353 patients)
Patients evaluated with
spirometry followed by
baseline bronchoscopy
(217 patients)
Patients evaluated with
follow-up bronchoscopy
(69 patients)
Female 120 (34.0) 67 (30.9) 22 (31.9)
Male 233 (66.0) 150 (69.1) 46 (68.1)
Caucasian 336 (95.2) 206 (94.9) 66 (95.7)
Black 15 (4.2) 9 (4.1) 2 (2.8)
Other 2 (0.6) 2 (1.0) 1 (1.4)
<60 years 132 (37.4) 80 (36.9) 30 (43.5)
60 - 69 years 125 (35.4) 84 (38.7) 25 (36.2)
70 years 96 (27.2) 53 (24.4) 14 (20.3)
Smoking Status
Never 25 (7.1) 15 (6.9) 4 (5.8)
Former 221 (62.6) 129 (59.4) 41 (59.4)
Current 106 (30.0) 73 (33.7) 24 (34.8)
Pack-years1 Mean (SD)† 50.8 (29.5) 50.5 (27.4) 50.5 (23.5)
Asbestos exposure (yes) 140 (39.7) 91 (41.9) 29 (42.1)
Lung cancer history (yes) 130 (36.8) 59 (27.2) 18 (26.1)
Reason for screening
Risk factors only* 161 (45.6) 100 (46.1) 33 (47.8)
Risk factors and symptoms** 192 (54.4) 117 (53.9) 36 (52.2)
Among patients with a history of smoking; *History of heavy smoking, asbestos exposure, previous aero-digestive cancer and clinical diagnosis of COPD;
**Symptoms include hemoptysis, persistent cough or progressive dyspnea.
Table 2. Adjusted risk estimates for detection of premalignant bronchial lesions or lung cancers based on the pulmonary
function test results in 217 high risk patients.
Normal All EPLs/Cancers1 Squamous MetaplasiaSquamous Dysplasia
(any grade) CIS/Invasive Cancer
Parameter N = 95
n (%) N = 122
n (%)
Adjusted OR2
(95% CI)
N = 91
n (%)
Adjusted OR2
(95% CI)
N = 25
n (%)
Adjusted OR2
(95% CI) N = 6
n (%)
Adjusted OR2
(95% CI)
80% 32 (33.7) 22 (18.0) Referent 18 (19.8)Referent 3 (12.0)Referent 2 (33.3) Referent
50% - <80% 48 (50.5) 58 (47.5) 1.58
(0.79 - 3.18) 43 (47.3)1.42
(0.67 - 3.00) 11 (44.0)2.17
(0.54 - 8.65) 3 (50.0) 2.09
(0.22 - 19.76)
<50% 15 (15.8) 42 (34.4) 4.56
(1.93 - 10.80) 30 (33.0)4.06
(1.62 - 10.15)11 (44.0)7.95
(1.77 - 35.67) 1 (16.7) 2.92
(0.12 - 68.10)
Ptrend3 0.001 0.003 0.005 0.47
Effect of Impaired Lung Function on the Development and Progression of Endobronchial Premalignant Lesions
70% 44 (50.6) 38 (33.3) Referent 33 (37.9)Referent 4 (19.0)Referent 1 (16.7) Referent
50% - <70% 32 (36.8) 47 (41.2) 1.83
(0.94 - 3.57) 31 (35.6)1.36
(0.66 - 2.79) 11 (52.4)3.35
(0.92 - 12.15) 4 (66.7) 9.81
(0.75 - 128.50)
<50% 11 (12.6) 29 (25.4) 3.29
(1.36 - 7.97) 23 (26.4)3.11
(1.25 - 7.72) 6 (28.6)5.08
(1.03 - 25.01) 1 (16.7) 8.77
(0.35 - 217.53)
Ptrend3 0.006 0.02 0.04 0.11
No/ Mild
COPD 50 (57.5) 41 (36.0) Referent 34 (39.1)Referent 5 (23.8)Referent 2 (33.3) Referent
COPD 23 (29.4) 37 (32.5) 2.03
(1.00 - 4.15) 25 (28.7)1.64
(0.76 - 3.52) 9 (42.9)3.27
(0.91 - 11.83) 3 (50.0) 4.89
(0.57 - 42.22)
Severe COPD 14 (16.1) 36 (31.6) 3.79
(1.67 - 8.64) 28 (32.2)3.70
(1.57 - 8.70) 7 (33.3)4.84
(1.15 - 20.43) 1 (16.7) 2.19
(0.13 - 37.94)
Ptrend 3 0.001 0.003 0.03 0.40
CI, confidence interval; OR, odds ratio; EPL, Endobronchial premalignant lesion; CIS, In-situ carcinoma. 1Includes pathological diagnoses—squamous meta-
plasia, dysplasia, carcinoma in-situ and invasive bronchial carcinoma; 2For overall analysis—adjusted for age at pulmonary function test, gender and pack-years
of smoking; 3p for trend; 4Mild COPD: (FEV1/FVC < 70% and FEV1 80%); Moderate COPD: (FEV1/FVC < 70% and 50% FEV1 80%); Severe COPD:
(FEV1/FVC < 70% and FEV1 < 50%); 5Patients who were missing either FEV1 or FVC information were not included in this analysis.
Table 3. Adjusted risk estimates for detection of premalignant bronchial lesions or lung cancers based on the pulmonary
function test results, stratified by gender.
Pulmonary Function
(N = 64)3
n (%)
(N = 86)3
n (%)
Adjusted OR2
(95% CI)
N = 31)3
n (%)
(N = 36)3
n (%)
Adjusted OR2
(95% CI)
80% 22 (34.4) 17 (19.8) Referent 10 (32.3) 6 (16.7) Referent
50% - <80% 34 (53.1) 43 (50.0) 1.43 (0.63 - 3.25)14 (45.2) 14 (38.9) 1.52 (0.40 - 5.75)
<50% 8 (12.5) 26 (30.2) 3.85 (1.34 - 11.10)7 (22.6) 16 (44.4) 6.54 (1.42 - 30.16)
Ptrend4 0.01 0.02
70% 32 (54.2) 28 (35.4) Referent 12 (42.9) 10 (28.6) Referent
50% - <70% 20 (33.9) 31 (39.2) 1.76 (0.79 - 3.93)12 (42.9) 16 (45.7) 1.93 (0.56 - 6.56)
<50% 7 (11.9) 20 (25.3) 3.59 (1.25 - 10.33)4 (14.3) 9 (25.7) 3.76 (0.74 - 19.04)
Ptrend4 0.02 0.10
No/Mild COPD 36 (61.0) 30 (38.0) Referent 14 (50.0) 11 (31.4) Referent
Moderate COPD 15 (25.4) 25 (31.6) 3.01 (0.85 - 4.76)8 (28.6) 12 (34.3) 1.98 (0.53 - 7.31)
Severe COPD 8 (13.6) 24 (30.4) 3.78 (1.40 - 10.19)6 (21.4) 12 (34.3) 4.54 (1.00 - 20.72)
Ptrend4 0.007 0.05
CI, confidence interval; OR, odds ratio; EPL, Endobronchial premalignant lesion; CIS, In-situ carcinoma. 1Includes pathological diagnoses—squamous meta-
plasia, dysplasia, carcinoma in-situ and and invasive bronchial carcinoma; 2For overall analysis—adjusted for pack-years of smoking and age at pulmonary
function test; 3Patients who were missing FEV1 or FVC information were excluded for certain analysis; 4p for trend; 5Mild COPD: (FEV1/FVC < 70% and
FEV1 80%); Moderate COPD: (FEV1/FVC < 70% and 50% FEV1 80%); Severe COPD: (FEV1/FVC < 70% and FEV1 < 50%).
Copyright © 2012 SciRes. JCT
Effect of Impaired Lung Function on the Development and Progression of Endobronchial Premalignant Lesions
Copyright © 2012 SciRes. JCT
to a higher grade [Hazard Ratio 2.48 (95% CI 0.65 -
9.41), p-value = 0.18)]. The mean time to progression
from a lower grade lesion to a higher grade was 27 months
for patients with COPD and 50 months for patients with-
out COPD (p = 0.02). The limited sample size precluded
more detailed analyses of histologic progresssion.
5. Discussion
Several previous studies have reported that ILF and
COPD are consistently associated with an increased risk
of incident LC [14-19]. ILF has also been shown to be
related to LC mortality [14,22,23]. Several mechanisms
are proposed to explain the relationship between im-
paired LF and incident LC. Chronic inflammation of the
airway and lung tissue is suggested to be the common
pathway in the development of COPD and/or LC [24,25].
Transactivation of genes involved in inflammation and
nuclear factor NF-κB activation can play an important
role in development of both LC and COPD [26]. Im-
paired mucociliary clearance associated with COPD re-
sults in decreased clearing of inhaled particulate matter
resulting in greater amount of carcinogens getting depos-
ited in the airway [25]. This prolonged contact of car-
cinogens to lung tissue may be a determinant in the de-
velopment of LC. This theory might have more credence
if the association between ILF and development and pro-
gression of EPLs can be demonstrated.
Few studies have examined the relationship between
ILF and EPLs. Prindiville et al. failed to identify any
increased risk of squamous atypia with greater degree of
airflow obstruction [27]. On the other hand, Kennedy et
al. reported a high prevalence of SD in patients with
COPD who reported at least 40 pack-years of smoking
[28]. Both of these studies used sputum cytology to de-
fine atypia/SD rather than histopathologic review of bi-
opsy specimens, as was done in our current study. Two
other studies have evaluated the prevalence of EPLs us-
ing autofluorescence bronchoscopy guided biopsies [7,
29]. While Breuer et al. noted no significant relation be-
tween COPD and the prevalence of EPLs (p = 0.40),
Lam et al. used linear predictors of LF measures and
reported that the risk of high-grade EPLs was greater in
patients with lower FEV1 volume and FEV1/FVC ratio
[29]. Consistent with Lam et al., our study results also
show that the patients with lower measures of LF were at
a greater risk of EPLs. In addition, the current study also
examines the risk of detecting EPLs using categorical
measures of LF and demonstrates a “dose-response” re-
lationship with greater level of LF impairment. While
Lam et al., noted statistically significant risk estimates
for EPLs in men and not in women, our results showed a
significant increase in risk among both genders. However,
considerable overlap in odds ratios prevents us from
evaluating the difference between the two genders.
The relationship between ILF and LC development has
previously been shown to be more pronounced with the
squamous cell subtype. In a study on patients undergoing
lung resection for non-small cell lung cancer (NSCLC),
impaired FEV1% was associated with significant in-
crease in risk for SCC subtype [17]. In another study,
Malhotra et al. also reported that impaired FEV1 was
associated with greater chance of SCC [30]. We observed
that ILF was associated with a 3 to 7 fold increased risk
of identifying SM and SD, precursors of SCC.
In addition to demonstrating a greater risk of EPL de-
tection with COPD, our results show that the mean time
to progression of the baseline lesions in COPD patients
was lesser than the non-COPD patients. Experimental
and modeling studies demonstrate total lung deposition
of inhaled particulate matter is much greater in patients
with obstructive disease compared to healthy individuals,
and the deposition enhancement is generally confined to
central airways [31,32]. This may explain the greater
prevalence and risk of progression for EPLs in the setting
of airflow obstruction. These patients could be a sub-
group that would require a more intense surveillance for
LC. However, it should be noted that in our study not all
patients had a follow-up biopsy limiting our ability to
perform detailed stratified analysis. Also, our study was
not powered to assess the risk of detecting invasive LC
or to evaluate the risk of progression in detail. In spite of
these limitations, our study provides preliminary evi-
dence that impaired lung function may increase the risk
of progression of EPLs.
6. Conclusion
The current study provides compelling evidence that im-
paired lung function is associated with a substantially
increased risk of developing EPLs. However, larger stud-
ies are needed to confirm and expand on these results,
and to evaluate progression rates among patients with air-
flow limitation. Overall, office spirometry can be a non-
invasive and inexpensive pre-screening tool to identify
patients with EPLs who need active surveillance for LC.
7. Acknowledgements
The authors would like to thank Wayne P. Slowik,
RRT/RPFT; Sandra J. Michel, RN BSN; and the Stacey
Scott Lung Cancer Registry team for their valuable con-
tribution in collecting, cleaning and maintaining clinical
information and PFT data.
This study was supported in part by the funding from
the Stacey Scott Lung Cancer Registry, Roswell Park
Cancer Institute
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