Cigarette Pack-years Research Articles

Lung function and plasma fibrinogen concentrations in the Newcastle Thousand Families birth cohort between age 49 and 51 years

A number of studies have suggested inverse associations between lung function and inflammatory markers, including fibrinogen. In this study, we used data from the Newcastle Thousand Families birth cohort to assess the association between contemporaneous markers of lung function and fibrinogen while adjusting for potential confounding factors throughout life. At age 49-51 years, complete data on lung function and plasma fibrinogen were available for 380 study members. These data were analysed in relation to each other, adjusted for sex and height, with further adjustment for potential confounders within linear regression models using robust estimates. Forced expiratory volume in 1 s was significantly inversely associated with plasma fibrinogen concentration after initial adjustments for sex and height (beta = -0.12, P = 0.011) and remained so after further adjustments for pack-years of cigarettes smoked and current smoking status. On further adjustment for standardized birthweight and duration breast-fed, the association approached statistical significance (P = 0.051). Adjusting for body mass index (BMI) resulted in a loss of significance (P = 0.09), but an unchanged regression coefficient, while, after adjustment for percent body fat, rather than BMI, the association was no longer significant (P = 0.20) and the coefficient reduced. The association between lung function and fibrinogen remains after adjustment for potential early-life confounders and smoking. However, it is not independent of contemporaneous measures of adiposity, with evidence of confounding by percent body fat. Further studies, with measures of adiposity, are required to confirm whether associations between markers of inflammation and lung function are due to residual confounding by adiposity.

Occupational exposure to crystalline silica and the risk of lung cancer in Canadian men

Crystalline silica is a recognized carcinogen, but the association with lung cancer at lower levels of exposure has not been well characterized. This study investigated the relationship between occupational silica exposure and lung cancer and the combined effects of cigarette smoking and silica exposure on lung cancer risk. A population-based case-control study was conducted in eight Canadian provinces between 1994 and 1997. Self-reported questionnaires were used to obtain a lifetime occupational history and information on other risk factors. Occupational hygienists assigned silica exposures to each job based on concentration, frequency and reliability. Data from 1681 incident lung cancer cases and 2053 controls were analyzed using logistic regression to estimate odds ratios (OR) and their 95% confidence intervals (CI). Models included adjustments for cigarette smoking, lifetime residential second-hand smoke and occupational exposure to diesel and gasoline engine emissions. Relative to the unexposed, increasing duration of silica exposure at any concentration was associated with a significant trend in lung cancer risk (OR ≥ 30 years: 1.67, 1.21-2.24; ptrend = 0.002). The highest tertile of cumulative silica exposure was associated with lung cancer (OR = 1.81, 1.34-2.42; ptrend = 0.004) relative to the lowest. Men exposed to silica for ≥30 years with ≥40 cigarette pack-years had the highest risk relative to those unexposed with <10 pack-years (OR = 42.53, 23.54-76.83). The joint relationship with smoking was consistent with a multiplicative model. Our findings suggest that occupational exposure to silica is a risk factor for lung cancer, independently from active and passive smoking, as well as from exposure to other lung carcinogens.

Occupational exposure to crystalline silica and the risk of lung cancer in Canadian men

Background: Crystalline silica is a highly prevalent occupational exposure and recognized human carcinogen, however its association with lung cancer remains contentious. Aims: We investigated the relationship between occupational silica exposure and lung cancer, and the combined effects of cigarette smoking and silica exposure on lung cancer risk. Methods: This was a population-based case-control study with 1681 incident lung cancer cases and 2053 controls from 8 Canadian provinces between 1994 and 1997. Self-reported questionnaires were used to obtain lifetime occupational history and information on other risk factors. Occupational hygienists, blinded to case-control status, assigned silica exposures to each job on based on concentration (low, medium, high); frequency (&lt;5%, 6-30%, &gt;30% of time in a typical week); and reliability (possible, probable, definite). Logistic regression was used to estimate odds ratios (OR) and their 95% confidence intervals. Four exposure metrics were modeled: ever exposure, concentration, duration, and cumulative exposure. Models were adjusted for cigarette smoking, exposure to second-hand smoke, and occupational exposure to diesel and gasoline. Results: A statistically significant trend in lung cancer risk was observed with increasing duration of exposure to silica at any concentration (OR for ?20 years=1.57, 1.22-2.03; ptrend=0.002), and persisted when exposures were restricted to low concentrations (OR for ?30 years=1.58, 1.15-2.16; ptrend=0.02). The highest tertile of cumulative silica exposure was associated with lung cancer (OR=1.41, 1.10-1.81; ptrend=0.04) relative to the lowest tertile. Men exposed to silica at low concentrations with ?40 cigarette pack-years had the highest risk relative to those unexposed with &lt;10 pack-years (OR=25.40, 17.21-37.50). The joint relationship with smoking was consistent with an additive model. Conclusions: Our findings suggest that occupational exposure to silica is an independent lung cancer risk factor.

OP04 Airway Obstruction and All-Cause and Respiratory Mortality: Exploring the Relationship between three Definitions of Obstruction, Smoking using Healths Survey for England and Scottish Health Survey Data

BackgroundDebate continues about the predictive value of different spirometry based definitions of chronic obstructive pulmonary disease (COPD). We explored the hazard of death for three overlapping definitions, and any significant...

Association Between Cataract and the Degree of Obesity

To investigate the association between the degree of obesity and cataract. We examined 3248 subjects (1421 men and 1827 women) aged 50 years and older who did not have a previous cataract operation. Data were derived from the fourth Korea National Health and Nutrition Examination Survey (2009). Cataract was evaluated by using Lens Opacities Classification System III. Body mass index was categorized into four groups (underweight, <18.5 kg/m(2); normal weight, 18.5 to 22.9 kg/m(2); overweight, 23.0 to 24.9 kg/m(2); and obese, ≥25.0 kg/m(2)). Association between the degree of obesity and cataract was evaluated using logistic regression analyses with adjustments of age, the total pack-years of cigarettes smoked, the amount of pure alcohol (g) consumed per day, daily time spent in vigorous physical activity, diabetes mellitus, sunlight exposure, education level, and income. Compared with the normal-weight group, the overweight group had significantly lower risk of any type of cataract (odds ratio, 0.70; 95% confidence interval, 0.50 to 0.97) in men and (odds ratio, 0.70; 95% confidence interval, 0.51 to 0.97) in women in the multiple logistic regression analyses. We could not find any unusual lifestyles or metabolic risks for explaining this low cataract prevalence in the overweight groups. However, nutrient intakes (e.g., vitamin B2, niacin, vitamin C, and vitamin A) were highest in the overweight group. The overweight group had significantly lower risk of cataract formation than the normal-weight group in Korean population.

Frequency of EGFR and KRAS mutations in patients with non small cell lung cancer by racial background: Do disparities exist?

IntroductionMutations in EGFR and KRAS can impact treatment decisions for patients with NSCLC. The incidence of these mutations varies, and it is unclear whether there is a decreased frequency among African Americans (AfAs). MethodsWe performed a retrospective chart review of 513 NSCLC patients undergoing EGFR and KRAS mutational analysis at the Hospital of the University of Pennsylvania between May 2008 and November 2011. Clinical and pathologic data were abstracted from the patients’ electronic medical record. ResultsOf 497 patients with informative EGFR mutation analyses, the frequency of EGFR mutation was 13.9%. The frequency of EGFR mutations was associated with race (p<0.001) and was lower in AfA patients compared to Caucasian (C) patients but did not reach statistical significance (4.8% vs. 13.7%, p=0.06). Mean Charlson Comorbidity Index and number of cigarette pack years were significantly lower in patients with EGFR mutations (p=0.01 and p<0.001, respectively). Multivariable logistic regression analysis showed a significant association between race and EGFR mutation (p=0.01), even after adjusting for smoking status (p<0.001) and gender (p=0.03). KRAS mutation (study frequency 28.1%) was not associated with race (p=0.08; p=0.51 for Afa vs. C patients), but was more common among smokers (p<0.001) and females (p=0.01). ConclusionsBased on multivariable analysis, even after adjusting for smoking status and gender, we found that race was statistically significantly associated with EGFR mutation, but not KRAS mutational status. To the best of our knowledge, this is the largest single institution series to date evaluating racial differences in EGFR and KRAS mutational status among patients with NSCLC.

Effects of Smoking, Depression, and Anxiety on Mortality in COPD Patients: A Prospective Study

Smoking, depression, and anxiety increase the risk of death in patients with COPD, but the combined effect of these factors is unknown. We assessed the interactive effects of smoking, depression, and anxiety on mortality in patients with COPD. We collected and analyzed data from 7,787 subjects with COPD, in 14 rural communities, from May 2008 to May 2012, and used logistic regression to evaluate the interactions and relative excess risk due to interaction (RERI). We applied the attributable proportion of interaction and the synergy index to evaluate the additive interactions of the factors. In our COPD subjects the interaction of current smoking and depression symptoms increased the death risk by 3.8-fold (odds ratio 3.78, 95% CI 2.51-5.05), with significant biological interactions (RERI 1.74, 95% CI 0.51-2.99, attributable proportion 0.48, 95% CI 0.13-0.85, synergy index 2.98, 95% CI 1.44-4.56). The biological interactions increased with increasing years or pack-years of smoking: for subjects with ≥ 30 years of smoking: RERI 1.80, 95% CI 1.05-2.75, attributable proportion 0.48, 95% CI 0.15-0.82, synergy index 2.85, 95% CI 1.75-3.96; for subjects with ≥ 40 pack-years of smoking: RERI 3.11, 95% CI 1.54-4.71, attributable proportion 0.60, 95% CI 0.31-0.91, synergy index 4.00, 95% CI 2.84-5.26. Similarly, the combined effect of current smoking and anxiety symptoms increased the death risk by 4.3-fold (odds ratio 4.27, 95% CI 95% CI 2.96-5.59), with significant biological interactions (RERI 1.51, 95% CI 0.31-2.74, attributable proportion 0.46, 95% CI 0.11-0.87, synergy index 2.89, 95% CI 1.31-4.51). The biological interactions also increased with increasing years or pack-years of smoking: for subjects with ≥ 30 years of smoking: RERI 1.41, 95% CI 0.45-2.43, attributable proportion 0.45, 95% CI 0.12-0.81, synergy index 2.88, 95% CI 1.24-5.98; for subjects with ≥ 40 pack-years of smoking: RERI 3.15, 95% CI 2.07-4.61, attributable proportion 0.55, 95% CI 0.21-0.94, synergy index 3.00, 95% CI 1.45-4.75. Smoking, depression, and anxiety are associated with higher risk of death in patients with COPD. The risk of death, depression, and anxiety increases with increasing duration of smoking (years) and cigarette pack-years. Chinese Clinical Trials Registration ChiCTR-TRC-12001958.

Interstitial lung abnormalities in a CT lung cancer screening population: prevalence and progression rate.

To determine the prevalence of interstitial lung abnormalities (ILAs) at initial computed tomography (CT) examination and the rate of progression of ILAs on 2-year follow-up CT images in a National Lung Screening Trial population studied at a single site. The study was approved by the institutional review board and informed consent was obtained from all participants. Image review for this study was HIPAA compliant. We reviewed the CT images of 884 cigarette smokers who underwent low-dose CT at a single site in the National Lung Screening Trial. CT findings were categorized as having no evidence of ILA, equivocal for ILA, or ILA. We categorized the type of ILA as nonfibrotic (ground-glass opacity, consolidation, mosaic attenuation), or fibrotic (ground glass with reticular pattern, reticular pattern, honeycombing). We evaluated the temporal change of the CT findings (no change, improvement, or progression) of ILA at 2-year follow-up. A χ(2) with Fisher exact test or unpaired t test was used to determine whether smoking parameters were associated with progression of ILA at 2-year follow-up CT. The prevalence of ILA was 9.7% (86 of 884 participants; 95% confidence interval: 7.9%, 11.9%), with a further 11.5% (102 of 884 participants) who had findings equivocal for ILA. The pattern was fibrotic in 19 (2.1%), nonfibrotic in 52 (5.9%), and mixed fibrotic and nonfibrotic in 15 (1.7%) of the 86 participants with ILA. The percentage of current smokers (P = .001) and mean number of cigarette pack-years (P = .001) were significantly higher in those with ILA than those without. At 2-year follow-up of those with ILA (n = 79), findings of nonfibrotic ILA improved in 49% of cases and progressed in 11%. Fibrotic ILA improved in 0% and progressed in 37% of cases. ILA is common in cigarette smokers. Nonfibrotic ILA improved in about 50% of cases, and fibrotic ILA progressed in about 37%.

Smoking as the potential link between Kimmelstiel-Wilson lesion and non-diabetic nodular glomerulosclerosis in male patients &amp;ndash; a single center retrospective study

The histological pattern of nodular glomerulosclerosis (NGS) can be found both in diabetic nephropathy (Kimmelstiel-Wilson (KW) lesion) and non-diabetic nodular glomerulosclerosis (non-diab NGS). Chronic smoking is considered to be a potential cause of non-diab NGS, but the prevalence of smokers in KW is unknown. In a retrospective analysis, native renal biopsy specimens (n = 644, 2001 - 2011) were evaluated and male patients' characteristics, including smoking habits, were assessed within three groups: diabetic patients with KW (n = 15), diabetic patients with other classes of diabetic nephropathy (non-KW; n = 46), and patients with non-diab NGS (n = 7). The majority of patients in the KW and non-diab NGS groups (13/15 = 87%, 7/7 = 100%, respectively; p = 1.0 vs. KW) were smokers, unlike the non-KW group (16/46 = 35%; p = 0.001 vs. KW). Cigarette pack-years showed a similar pattern (KW: 15 (6 - 30), non-KW: 0 (0 - 21), non-diab NGS: 30 (16 - 33); p = 0.010 non-KW vs. KW, p = 0.008 non-KW vs. non-diab NGS). Other known factors responsible for the worsening of non-KW or the development of non-diab NGS did not differ in the groups (age, body mass index, duration of diabetes mellitus, HbA1c, prevalence of hypertension, duration of hypertension, serum cholesterol, triglyceride, estimated glomerular filtration rate, and renin-angiotensin-aldosteron system-blocker treatment). We propose that chronic cigarette smoking could play a pivotal role in the development of KW lesions.

Interactions between Cigarette Smoking and Polymorphisms of Xenobiotic-Metabolizing Genes: The Risk of Oral Leukoplakia

Background: This case-control study investigates the role of xenobiotic-metabolizing genes, including glutathione S-transferases (GSTs) and cytochrome P450 1A1 (CYP1A1) and 2E1 (CYP2E1), in the susceptibility to oral potentially malignant disorders (OPMDs).Methods: The genotypes of GSTM1, GSTT1, GSTP1, CYP1A1∗2C, and CYP2E1 PstI/RsaI polymorphisms were determined for 217 OPMD cases and 492 age- and sex-matched controls from a Taiwanese penitentiary.Results: Compared to the GSTM1-present genotype, the GSTM1-null genotype was significantly associated with increased risk of leukoplakia (odds ratio [OR]=1.46, 95% l [CI]=1.01–2.10). Similarly, compared to the CYP1A1∗2C A/G+G/G genotype, the CYP1A1∗2C A/A genotype was significantly associated with increased risk of leukoplakia (OR=1.64, 95% CI=1.12–2.40), particularly for smokers consuming &gt; 13 pack-years of cigarettes (OR=2.40, 95% CI=1.40–4.11) (Interaction P=0.039). In addition, participants with 4–5 risk genotypes (OR &gt; 1) experienced higher risks for leukoplakia than those with 0-1 risk genotypes (OR=3.19, 95% CI=1.65–6.15) (Trend test P=0.001).Conclusions: Our findings suggest that the CYP1A1∗2C A/A genotype may increase the risk of leukoplakia, especially for heavy smokers. Xenobiotic-metabolizing genes may simultaneously modulate this disease risk. These observations require further confirmation with larger samples.

Interactions between cigarette smoking and polymorphisms of xenobiotic-metabolizing genes: the risk of oral leukoplakia.

Background: This case-control study investigates the role of xenobiotic-metabolizing genes, including glutathione S-transferases (GSTs) and cytochrome P450 1A1 (CYP1A1) and 2E1 (CYP2E1), in the susceptibility to oral potentially malignant disorders (OPMDs).Methods: The genotypes of GSTM1, GSTT1, GSTP1, CYP1A1∗2C, and CYP2E1 PstI/RsaI polymorphisms were determined for 217 OPMD cases and 492 age- and sex-matched controls from a Taiwanese penitentiary.Results: Compared to the GSTM1-present genotype, the GSTM1-null genotype was significantly associated with increased risk of leukoplakia (odds ratio [OR]=1.46, 95% l [CI]=1.01–2.10). Similarly, compared to the CYP1A1∗2C A/G+G/G genotype, the CYP1A1∗2C A/A genotype was significantly associated with increased risk of leukoplakia (OR=1.64, 95% CI=1.12–2.40), particularly for smokers consuming > 13 pack-years of cigarettes (OR=2.40, 95% CI=1.40–4.11) (Interaction P=0.039). In addition, participants with 4–5 risk genotypes (OR > 1) experienced higher risks for leukoplakia than those with 0-1 risk genotypes (OR=3.19, 95% CI=1.65–6.15) (Trend test P=0.001).Conclusions: Our findings suggest that the CYP1A1∗2C A/A genotype may increase the risk of leukoplakia, especially for heavy smokers. Xenobiotic-metabolizing genes may simultaneously modulate this disease risk. These observations require further confirmation with larger samples.

COPD-Screening in der hausärztlichen Praxis mit einem Lungenfunktions-Schnellmessgerät

Screening measures can facilitate the diagnosis of chronic obstructive pulmonary disease (COPD) and help save costs and time. We examined whether use of a lung function screener (Vitalograph copd-6™) can help general practitioners to identify patients at risk for COPD. In 17,856 patients aged > 40 years (smokers/ex-smokers with cough and/or exertional dyspnoea) general practitioners measured prebronchodilator FEV1 [% of predicted] and FEV1/FEV6 with the lung function screening device. In addition, the general practitioners completed a questionnaire on symptoms, history and planned measures and estimated whether or not the patient was at risk for COPD. In 2927 patients (16.7 %) an FEV1/FEV6 < 70 % was measured; 88.2 % of these were classed by the doctors as being at risk for COPD. The total number of all patients with suspected COPD was considerably greater (10,000; 56 % of the total population); in only 25.3 % was an FEV1/FEV6 < 70 % documented. Compared with patients without a suspicion of COPD, patients judged to be at risk for COPD in spite of an FEV1/FEV6 ≥ 70 % were more often male, had more cigarette pack years and more often had dyspnoea, but less often cough, as main symptom. They had more concomitant diseases and previous hospitalisations, more prescriptions for bronchodilators, glucocorticoids and antibiotics in the past year and lower FEV1 values. In 61.3 % of the patients with suspected COPD the general practitioners planned further evaluation by spirometry, in 39.9 % referral to a pulmonologist as alternative or additional procedures were suggested. Most patients with an FEV1/FEV6 < 70 % measured with the lung function screener Vitalograph copd-6™ were classed by the general practitioners as being at risk for COPD. Even in patients with unremarkable FEV1/FEV6 values the diagnosis of suspected COPD was often made if clinical signs or symptoms or a reduced FEV1 pointed to such a suspicion.

Abstract B79: Tobacco smoking, polymorphisms in xenobiotic metabolism enzyme genes, and prostate cancer risk and survival

Abstract Introduction: The association between tobacco smoking and prostate cancer (PCa) risk and progression remains unclear. This study examined the association between tobacco smoking and risk of localized and advanced PCa, PCa-specific mortality, and overall mortality in African-American, Hispanic and non-Hispanic White men. Polymorphisms in xenobiotic metabolism enzyme genes were further examined as possible modifiers of associations with smoking. Methods: Using data from the California Collaborative Prostate Cancer Study, a multiethnic population-based case-control study conducted in Los Angeles County (631 advanced and 533 localized cases; 594 controls) and the San Francisco Bay Area (568 advanced and 208 localized cases; 545 controls), we evaluated associations between tobacco smoking and risk of localized and advanced PCa using conditional logistic regression. Cox proportional hazards regression models and Kaplan Meier curves with log-rank tests were used to assess associations with PCa-specific and all-cause mortality. Median follow-up time for cases was 8.8 years (IQR: 6.2-9.9). We also investigated the role of 12 metabolism enzyme single nucleotide polymorphisms from 7 genes as potential modifiers of the relationship between tobacco smoking and PCa risk and progression using interaction models. Results: After adjusting for age, PCa family history, body mass index, alcohol consumption, intake of meat cooked at high temperature, and use of snuffing/chewing tobacco, non-Hispanic Whites who were former smokers had an increased risk of localized PCa when compared to never smokers (OR=1.52, 95%CI: 1.11-2.09, p&amp;lt;0.01). Risk increased with younger age at first tobacco use (p-trend&amp;lt;0.01), duration of tobacco smoking (p-trend=0.01), number of daily cigarettes smoked (p-trend=0.02), and cigarette pack-years (p-trend=0.03). Current smoking was associated with an increased risk of advanced PCa (OR=1.41, 95%CI: 1.02-1.94, p=0.037) among non-Hispanic Whites, but a decreased risk among Hispanics (OR=0.48, 95%CI: 0.23-0.99, p=0.047). No significant trends were seen for any of the smoking variables among Hispanics or African-Americans. A CYP1A2 polymorphism (rs7662551) modified the relationship between smoking status and PCa risk; the addition of each C-allele increased risk for localized (p-interaction=0.01) and advanced (p-interaction=0.03) PCa, particularly among current smokers. Tobacco smoking was not associated with PCa-specific mortality. For all-cause mortality, increased risk was associated with current smoking, duration of smoking, cigarette pack-years, and young age at first smoking. Kaplan Meier survival probabilities for current smokers were 77% from all-cause mortality and 89% from PCa-specific mortality. Conclusions: We observed that tobacco smoking was associated with risk of localized and advanced PCa primarily among Non-Hispanic Whites. Moreover, we observed that tobacco smoking was associated with all-cause mortality, albeit no associations were observed for PCa-specific mortality. Genetic variation in CYP1A2 seems to modify the relationship of tobacco smoking status and PCa risk, but not mortality. Citation Format: Ahva Shahabi, Roman Corral, Chelsea Catsburg, Amit D. Joshi, Jocelyn Koo, Esther M. John, Sue A. Ingles, Mariana C. Stern. Tobacco smoking, polymorphisms in xenobiotic metabolism enzyme genes, and prostate cancer risk and survival. [abstract]. In: Proceedings of the Eleventh Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2012 Oct 16-19; Anaheim, CA. Philadelphia (PA): AACR; Cancer Prev Res 2012;5(11 Suppl):Abstract nr B79.

Abstract A71: Smoking and breast cancer survival among New Mexican Hispanic and non-Hispanic white women.

Abstract The association of smoking with breast cancer mortality is not well established. Results from the few studies to date are mixed. Data for ethnic minorities are sparse. The current study examined the association of active cigarette smoking with breast cancer and non-breast cancer mortality in a pooled sample of 1,368 New Mexico Hispanic women (n=556) and non-Hispanic white (NHW) women (n=812) diagnosed with a first primary invasive breast cancer from two case-control studies: the New Mexico Women's Health Study (NMWHS: 1992-1994) and the 4-Corner's Breast Cancer Study (4-CBCS: 1999-2004). The cases were ascertained by the New Mexico Tumor Registry. Baseline data were collected for smoking exposure and other relevant covariates (age, study, alcohol intake, body mass index, menopausal status, family history, parity, energy intake and expenditure). The National Death Index was used to determine vital status through December 31, 2008. A total of 312 deaths occurred over an average of 9.2 years of follow-up (NMWHS, 12.4; 4-CBCS, 7.2); 188 were breast cancer deaths. The prevalence of current and former smoking was 13% and 25% in Hispanic women compared to 16% and 32% in NHW women. Thirty-three percent of NHW women smoked for more than 13 pack-years versus 16% of Hispanic women. Hazard ratios were calculated using Cox Proportional analysis adjusting for the covariates. Cigarette smoking status (former, current) and pack-years were not associated with breast cancer mortality in Hispanic women. However, there was a non-significant positive association in NHW women who smoked (current: HR, 1.42, 95% CI 0.83-2.41; pack-years &amp;gt;13: HR, 1.42; 95% CI 0.90-2.24). In contrast, there were significant positive associations with non-breast cancer mortality in H women (pack-years &amp;gt;13: HR, 2.95; 95% CI 1.52-5.75) and NHW women (pack-years &amp;gt;13: HR, 2.08; 95% CI 1.25-3.45). These results do not support an association of smoking with breast cancer mortality, particularly in Hispanic women. However, smoking is significantly associated with non-breast cancer mortality in women diagnosed with breast cancer. Citation Format: Kathy B. Baumgartner, Christina Pinkston, Avonne Connor, Stephanie Denkhoff, Dongyan Yang, Richard N. Baumgartner. Smoking and breast cancer survival among New Mexican Hispanic and non-Hispanic white women. [abstract]. In: Proceedings of the Fifth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2012 Oct 27-30; San Diego, CA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2012;21(10 Suppl):Abstract nr A71.

Changes in Body Weight and Adiposity Predict Periodontitis Progression in Men

Most studies linking obesity and periodontal disease have been cross-sectional in design. We examined whether gains in body weight, waist circumference, and arm fat area are associated with periodontitis progression in 893 non-diabetic men followed for up to four decades in the prospective VA Dental Longitudinal Study. Probing pocket depth (PPD) was measured by calibrated examiners. Repeated-measures generalized linear models estimated the mean cumulative numbers of teeth with PPD events (PPD > 3 mm) at each dental examination and the slopes associated with increasing numbers of affected teeth over time. Means were adjusted for baseline PPD, education, and cigarette pack-years, and time-dependent values of age, mean plaque score, cigarette packs/day, brushing, and flossing. Men who were overweight at baseline and gained weight most rapidly (> 0.19 kg/yr or ~15 lb during follow-up) had significantly more PPD events than men in the lowest tertile of weight gain (≤ -0.05 kg/yr). Overweight men whose waist circumference increased > 0.14–0.39 or > 0.39 cm/yr experienced more PPD events than men in the lowest tertile (≤ 0.14 cm/yr). Increase in arm fat area was associated with disease progression in normal-weight men. These results suggest that tracking adiposity changes with easily obtained anthropometric measures may help predict risk of periodontitis progression.

Cumulative exposure to stimulants and immune function outcomes among HIV-positive and HIV-negative men in the Multicenter AIDS Cohort Study.

We examined associations between stimulant use (methamphetamine and cocaine) and other substances (nicotine, marijuana, alcohol and inhaled nitrites) with immune function biomarkers among HIV-seropositive (HIV +) men taking highly active antiretroviral therapy (ART) and HIV-seronegative (HIV-) men in the Multicenter AIDS Cohort Study. Among HIV + men, cumulative adherence to ART (4.07, 95% confidence interval [CI]: 3.52, 4.71, per 10 years of adherent ART use), and recent cohort enrolment (1.38; 95% CI: 1.24, 1.55) were multiplicatively associated with increase in CD4+/CD8+ ratios. Cumulative use of methamphetamine (0.93; 95% CI: 0.88, 0.98, per 10 use-years), cocaine (0.93; 95% CI: 0.89, 0.96, per 10 use-years) and cumulative medical visits (0.99; 95% CI: 0.98, 0.99, per 10 visit-years), each showed small negative associations with CD4+/CD8+ ratios. Among HIV- men, cumulative medical visits (0.996; 95% CI: 0.993, 0.999), cumulative number of male sexual partners (0.999; 95% CI: 0.998, 0.9998, per 10 partner-years) and cigarette pack-years (1.10; 95% CI: 1.02, 1.18, per 10 pack-years) were associated with CD4+/CD8+ ratios over the same period. ART adherence is associated with a positive immune function independent of stimulant use, underscoring the influence of ART on immune health for HIV+ men who engage in stimulant use.

Opium Could Be Considered an Independent Risk Factor for Lung Cancer: A Case-Control Study

Background: Lung cancer is the leading cause of cancer-related death worldwide, and half of all incident lung cancers are believed to occur in the developing countries, including Iran. Objective: We investigated the association of opium with the risk of lung cancer in a case-control study. Methods: We enrolled 242 cases and 484 matched controls in this study. A questionnaire was developed, containing questions on basic demographic characteristics, as well as lifelong history of smoking cigarettes, exposure to passive smoking, opium use and alcohol consumption. For smoking cigarettes and opium and also oral opium intake frequency, duration and cumulative use were categorized into three groups: no use, low use and high use. Conditional logistic regression was used to calculate the odds ratios (ORs) and 95% confidence intervals (CIs). Results: Multivariate analysis in men showed that after adjusting for the effect of ethnicity, education and pack years of smoking cigarettes, smoking opium remained as a significant independent risk factor with an OR of 3.1 (95% CI 1.2–8.1). In addition, concomitant heavy smoking of cigarettes and opium dramatically increased the risk of lung cancer to an OR of 35.0 (95% CI 11.4–107.9). Conclusion: This study demonstrated that smoking opium is associated with a high risk of lung cancer as an independent risk factor.

Abstract 178: RCBTB1 Genotypes Modulate Smoking Effect on Carotid Intima-Media Thickness: A Finding from a Genome-Wide Interaction Analysis

Objective: Smoking is an established risk factor for atherosclerotic disease. However, the degree of the cigarette smoking-induced damage varies from individual to individual, partly due to the between-individual difference in genetic makeup. The aim of this study was to identify genetic loci influencing the effect of cigarette smoking on carotid intima-media thickness (IMT) by performing a genome-wide association smoking-by-SNP interaction analysis. Methods and results: Genome-wide genotyping was performed using the Affymetrix SNP array 6.0 among 1,010 individuals who underwent B-mode ultrasound examination of carotid IMT from the population-based Northern Manhattan Study. Cigarette pack-years was calculated as number of years smoked multiplied by number of cigarettes smoked per day, then divided by 20. After quality control, a total of 722,379 single nucleotide polymorphisms (SNPs) were included in the final analysis. Generalized linear modeling was conducted to look for smoking-by-SNP interaction on carotid IMT while controlling for age, sex, hypertension, diabetes, dyslipidemia, body mass index, waist-to-hip ratio, and the top 3 principal components estimated to capture ancestry by EIGENSTRAT. Ten SNPs near or within 5 genes showed an interactive effect with cigarette smoking on IMT with a p value &lt;1.0E-5. Among them, 3 SNPs (including 1 exonic splice enhancer SNP rs3751283, P=8.3E-7) are near or within regulator of chromosome condensation and BTB domain containing protein 1 (RCBTB1) gene on 13q14. Specifically, for SNP rs3751283, the mean IMT was substantially increased among CC-carriers (0.70 mm, 0.76 mm, 0.81 mm for 0, &lt;20, and ≥20 cigarette pack-years, respectively, P=2.6E-6), slightly increased with smoking pack-years among TC-carriers (0.72 mm, 0.74 mm, 0.75 mm for 0, &lt;20, and ≥20 cigarette pack-years, respectively, P=0.03), but very similar (0.73 mm) among TT-carriers for the three smoking groups (P=0.84). Conclusion: Our genome-wide interaction analysis reveals multiple genes, especially RCBTB1, that may modify the effect of smoking on carotid IMT. These genes will be further evaluated in our full dataset with additional genotyping. Also, larger independent studies are needed to validate these findings.

Abstract 664: Menthol cigarettes in relation to breast cancer incidence in African American women

Abstract The Tobacco Products Scientific Advisory Committee has found that smokers of menthol cigarettes have an earlier age at smoking initiation, less success in smoking cessation, and are more likely to be African American than smokers of non-menthol cigarettes. However, whether menthol cigarettes are associated with higher cancer risk relative to non-menthol cigarettes is unclear. Recent studies of smoking and breast cancer suggest that long-term smoking may associated with a small increase in risk, but no data are available on type of cigarette. We assessed the relative effects of menthol and non-menthol cigarettes on incidence of breast cancer in a large prospective cohort of African American women. The Black Women's Health Study has followed approximately 59,000 women with biennial questionnaires since enrollment in 1995. Beginning in 2003, data has been collected on whether cigarettes smoked were menthol or non-menthol; menthol cigarettes were reported by 64.7% of smokers who provided information. During follow-up from 2003 through 2010, 739 incident breast cancer cases occurred. In proportional hazard models that controlled for age and numerous breast cancer risk factors, hazard ratios (HR) were computed for categories of pack-years of smoking of the two types of cigarettes relative to a reference group of never-smokers who reported no regular exposure to second-hand smoke. The HR for β20 pack-years of smoking non-menthol cigarettes was 1.70 (95% confidence interval (CI) 1.04-2.76); for β20 pack-years of smoking menthol cigarettes, the HR was 1.14 (95% CI, 0.72-1.82). Our findings suggest that, to the extent that higher pack-years of smoking may be associated with breast cancer, smoking menthol cigarettes is not more harmful than smoking non-menthol cigarettes. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 664. doi:1538-7445.AM2012-664

Abstract 5478: Indoor coal smoke exposure, tobacco use, and lung cancer risk in Xuanwei, China

Abstract Introduction: Lung cancer rates in Xuanwei County, Yunnan Province are among the highest in China. We have previously reported that indoor combustion of smoky coal for home heating and cooking was associated with increased risk of lung cancer and that this effect varies markedly by coal type. Further, improved stove ventilation is followed by reduction in lung cancer risk. We explored the joint relationship between tobacco use and coal use in Xuanwei men. Methods: We analyzed data from a population-based case-control study of lung cancer in Xuanwei. Cases were identified from four Xuanwei hospitals and controls were selected from the general population by probability sampling. Controls were matched one-to-one with cases on age. In total, 260 cases and 260 controls were analyzed in this study. Tobacco, coal, and solid fuel exposures were tabulated from questionnaires and reported in cigarette pack-years, duration of smoking, and average tons of coal used annually. Odds ratios and 95% confidence intervals were estimated by conditional logistic regression with the main effects of coal, smoking, and coal-smoking interaction terms. Results: Overall, smoking was positively and significantly, although only modestly, associated with lung cancer risk (OR per pack-year: 1.02; 95% CI: 1.01-1.04). The risk of lung cancer per pack-year of smoking decreased as cumulative lifetime use of smoky coal increased (0-50 tons coal: OR: 1.07; 95% CI: 1.01-1.15; &amp;gt;50-150 tons coal: OR: 1.05; 95% CI: 1.01-1.10; &amp;gt;150 tons coal: OR: 1.00; 95% CI: 0.99-1.03; P-interaction: 0.041). Discussion: Our results suggest that the effect of tobacco on lung cancer risk was weaker in men exposed to higher amounts of coal. Results are consistent with previous cohort study findings in Xuanwei. Constituents of coal combustion, such as polycyclic aromatic hydrocarbons, could plausibly act to diminish the carcinogenicity of tobacco through metabolic competition or other possible mechanisms. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 5478. doi:1538-7445.AM2012-5478