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1 lung tumorigenesis between light smokers and heavy smokers.
2 g (P < 0.05), with higher risks reported for heavy smokers.
3 r moderate smokers, and 1.57 (1.47-1.66) for heavy smokers.
4 25, 9.17, and 11.89 for light, moderate, and heavy smokers.
5 increased lung cancer risk, especially among heavy smokers.
6 phrenic, 26 depressed, and 26 nonpsychiatric heavy smokers.
7  beta-carotene supplements except in current heavy smokers.
8 ht smokers 0.847 (95% CI = 0.824-0.871), and heavy smokers 0.732 (95% CI = 0.708-0.752).
9 was lowest in nonsmokers and highest in very heavy smokers (18.5% vs 34.5%, P < 0.001).
10  in nonsmokers and 0.69 (95% CI, 0.4-1.2) in heavy smokers (80 pack-years; P < 0.01 for the interacti
11 pmol/mmol, mean +/- SEM) was 176.5+/-30.6 in heavy smokers, 92.7+/-4.8 (P<.05) in moderate smokers, a
12 erformed for lung cancer screening in older, heavy smokers, a simple visual assessment of CAC can be
13  never, 42.3% former, 10.6% light, and 11.1% heavy smokers according to self-report.
14 ngs of this pilot study demonstrated that in heavy smokers, adjunctive systemic AZM in combination wi
15                            Among 543 current heavy smokers, adjusted mean values of FEV1 (lowest to h
16 T) was used to screen 2994 current or former heavy smokers, aged 50-74 years, for lung cancer.
17 V1, and 5002 with high FEV1 from each of the heavy smoker and never smoker groups.
18 h smoking reduction was mostly evident among heavy smokers and for cardiovascular disease mortality.
19 here were no significant differences between heavy smokers and light smokers in EDV (p = 0.52), basal
20 haring of genetic causes of low FEV1 between heavy smokers and never smokers (p=2.29 x 10(-16)) and b
21 soriasis risk was particularly augmented for heavy smokers and persons with longer durations of smoki
22 ls exposed to high oxidative stress, such as heavy smokers, and those with poor nutrition.
23 can be safely performed in healthy subjects, heavy smokers, and those with severe obstructive airflow
24                           The risk model for heavy smokers can allow us to stratify heavy smokers int
25 iod, assuming a 50% stage shift, the current heavy smoker cohort had 553 fewer lung cancer deaths (13
26 ark-colored irises (P < 0.009), and lower in heavy smokers compared to light (P < 0.0045) and never (
27 or lung cancer subtypes, the excess risk for heavy smokers compared with never smokers was higher for
28 ted increased dopamine synthesis capacity in heavy smokers compared with non-smokers.
29 w-dose CT data were evaluated in a cohort of heavy smokers consecutively recruited by the Multicentri
30 s from CARET participants (current or former heavy smokers), consisting of 100 patients who subsequen
31 rs with cancer risks as high as those within heavy smokers could be identified.
32                                              Heavy smokers could be successfully distinguished from n
33 er-smokers from 43 studies, we extracted the heavy smokers (CPD >20) and light smokers (CPD </=10) wi
34 ed to vary by age, with the odds ratio among heavy smokers decreasing from 2.8 among 32- to 44-year-o
35                                              Heavy smokers defined by prediagnostic circulating cotin
36                                              Heavy smokers displayed an increased relative risk (RR)
37 osed to more nicotine per cigarette than are heavy smokers due to more frequent, intensive puffing.
38 f colorectal cancer were elevated among male heavy smokers exposed to asbestos.
39 in the screening of older current and former heavy smokers for early detection of lung cancer, which
40 actions of TCF4 genotype and smoking status; heavy smokers (FTND score >/= 4) showed stronger gene ef
41 ntrols, with smoking exposure categorized as heavy smoker (&gt;/=10 pack-years) versus never smoker/<10
42 ncrease cessation rates only for moderate to heavy smokers (&gt; or = 15 cigarettes/d).
43       The estimated odds ratio among the 350 heavy smokers (&gt; or = 50 pack-years) was 1.41 (95% confi
44  light smokers (< or =1 pack/week) and eight heavy smokers (&gt; or =1 pack/day), and their sera were ad
45 ancer, respectively, and only 39% and 49% of heavy smokers (&gt; or =40 cigarettes per day) acknowledged
46 ons were defined: never smokers (0 pack-yr), heavy smokers (&gt;/= 13 pack-yr) and light smokers (< 13 p
47 1 ng/mL), light smokers (3.1-20.9 ng/mL), or heavy smokers (&gt;/= 21.0 ng/mL).
48 not change above 20 CPD and was 36% lower in heavy smokers (&gt;/=20 CPD) than in lighter smokers (<20 C
49  mortality similar to that of quitters among heavy smokers (&gt;/=21 cigarettes/day) who reduced their s
50 r, former, light (</=10 cigarettes/day), and heavy smokers (&gt;10 cigarettes/day) according to self-rep
51 in plasma (V(T)/f(P)) in 10 nonsmokers and 6 heavy smokers (&gt;14 cigarettes/d; abstinent for >36 h).
52 48.3%, P<0.05), but recipients of lungs from heavy smokers (&gt;40 pack-years smoking history) exhibited
53                                              Heavy smokers (&gt;40 pack-years) had increased risk for ca
54 moderate smokers (20 to <40 pack-years), and heavy smokers (&gt;or=40 pack-years).
55 [RRR] = 2.1) and severe CAL (RRR = 3.4), and heavy smokers had a higher risk for moderate (RRR = 3.0)
56 ls measured within 5 years before diagnosis, heavy smokers had a multivariable-adjusted HR for death
57  From the neutral to the cigarette cue scan, heavy smokers had greater increases than nonsmoking cont
58 y (aHR, 1.08; 95% CI, 0.96-1.20), but former heavy smokers had higher risk for both HF (aHR, 1.45; 95
59 , when compared with current smokers, former heavy smokers had lower risk of death (aHR, 0.64; 95% CI
60 ith >15 years of cessation, of whom 312 were heavy smokers (highest quartile; >/=32 pack-years).
61 y cigarette consumption at the initial exam: heavy smokers (HS) > or = 20 cigarettes/day (n = 31); li
62 smokers were significantly more likely to be heavy smokers in adulthood (odds ratio [OR] = 1.45; 95%
63  short-term cessation success in moderate to heavy smokers in each survey year.
64  compared with local survey-derived data for heavy smokers in New York City.
65 l for heavy smokers can allow us to stratify heavy smokers into subgroups with distinct risks, which,
66 tory volume in 1 s (FEV1) distribution among heavy smokers (mean 35 pack-years) and never smokers.
67 an age 52 yr), predominantly male (78%), and heavy smokers (mean 56 pack-yr).
68 .96, 1.93) when compared with that for CARET heavy smokers not exposed to asbestos, after adjusting f
69 0.7-0.9]), with an adjusted hazard ratio for heavy smokers of 0.5 (95% CI=0.3-0.9) compared to that o
70 eriodontal health and reducing tooth loss in heavy smokers of cigarettes, cigars, and pipes with peri
71 ment therapy may be particularly helpful for heavy smokers or smokers who have experienced multiple f
72 (OR = 0.19; 95% CI, 0.06-0.59) compared with heavy smokers (OR = 0.83; 95% CI, 0.41-1.69).
73  smokers (OR, 2.1; CI, 1.3-3.3), but not for heavy smokers (OR, 1.0; CI, 0.7-1.5).
74     Similarly, this risk was more evident in heavy smokers (OR, 2.55; 95% CI, 1.61-4.03) than in ligh
75 okers, OR = 1.84 (95% CI: 1.2, 2.9); and for heavy smokers, OR = 1.85 (95% CI: 1.0, 3.5), relative to
76 icantly lower in light smokers compared with heavy smokers (p < 0.006 and p < 0.004, respectively).
77 tooth loss (P = 0.000), BOP (P = 0.004), and heavy smokers (P = 0.001).
78 light smokers (P = 5.15 x 10(-5)) but not in heavy smokers (P = 0.52).
79 n low-dose computed tomography scans in male heavy smokers participating in a lung cancer screening s
80          These associations were stronger in heavy smokers, particularly for IL1B C3954T (OR, 1.59; 9
81 n (healthy volunteers, patients with asthma, heavy smokers, patients undergoing lung volume reduction
82  moderate smokers (RR = 0.92; 0.72-1.16) and heavy smokers (RR = 0.95; 0.74-1.24), and did not change
83                              In both trials, heavy smokers seem to be the most adversely affected gro
84 were observed when we investigated light and heavy smokers separately.
85 s were most pronounced in non-smokers, while heavy smokers showed reduced levels of IL-1alpha protein
86 udies, especially for adenocarcinoma and for heavy smokers, suggesting that more emphasis should be p
87 ioeconomic status (OR = 4.5), in moderate or heavy smokers than nonsmokers (OR = 3.1), and in subject
88                                We identified heavy smokers that were resistant (n = 65) or susceptibl
89 less likely than younger, more educated, and heavy smokers to perceive an increased personal risk of
90 ST randomized 53,454 older current or former heavy smokers to receive LDCT or chest radiography (CXR)
91                                       Former heavy smokers were defined as individuals who have smoke
92  5.18, respectively, for light, moderate, or heavy smokers, whereas among the individuals from famili
93  considered as a risk-reduction strategy for heavy smokers who cannot quit abruptly.
94                                       Twenty heavy smokers (who smoked > or =20 cigarettes per day) a
95                                Compared with heavy smokers with a low seafood/fish intake, light smok
96  brushes from the bronchial epithelium of 35 heavy smokers without cancer.

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