Pack-years Of Cigarette Smoking Research Articles

Associations of smoking status with carotid atherosclerosis: Mediated role of blood indexes and blood pressure

Background and aimsWe aimed to assess the relationship between smoking status and carotid atherosclerosis (CA) with different manifestations and to explore the underlying mechanisms. Methods and resultsA total of 60,655 middle-aged and elderly participants were recruited. Logistic regression models were used to examine the association of smoking, various blood indexes [i.e., blood pressure, blood lipid, glycated hemoglobin (HbA1c) and homocysteine (Hcy)] with CA in different manifestations including carotid intima-media thickness (cIMT), plaques, and stenosis. Compared with nonsmokers, current smokers were associated with a higher prevalence of CA (OR = 3.48, 95%CI: 3.21–3.77) and its specific manifestations including cIMT (OR = 2.66, 95%CI: 2.42–2.93), plaques (OR = 3.67, 95%CI: 3.35–4.02) and stenosis (OR = 2.04, 95%CI: 1.64–2.54), after adjusting for potential confounders. Former smokers were also associated with an increased prevalence of CA (OR = 1.82, 95%CI: 1.54–2.14), cIMT (OR = 1.39, 95%CI: 1.14–1.69), plaques (OR = 2.04, 95%CI: 1.71–2.44) and stenosis (OR = 1.72, 95%CI: 1.18–2.51), but the associations were consistently weaker than that of the current smokers. The prevalence of CA, cIMT, plaques and stenosis among current smokers was positively associated with pack-years of cigarette smoking, partially mediated by SBP, HbA1c, TG, HDL-C and Hcy with a mediated proportion of 1.12%, 3.28%, 6.33%, 6.01% and 12.7%, respectively. Stratified analysis by sex showed a significantly higher CA among the current male smokers than females. ConclusionsCurrent and former smoking was associated with increased carotid atherosclerosis, predominantly by current male smokers. A positive gradient between pack-years and carotid atherosclerosis among current smokers is partially mediated by SBP, HbA1c, TG, HDL-C and Hcy.

Examining the Effect of Genes on Depression as Mediated by Smoking and Modified by Sex.

Depression is heritable, differs by sex, and has environmental risk factors such as cigarette smoking. However, the effect of single nucleotide polymorphisms (SNPs) on depression through cigarette smoking and the role of sex is unclear. In order to examine the association of SNPs with depression and smoking in the UK Biobank with replication in the COPDGene study, we used counterfactual-based mediation analysis to test the indirect or mediated effect of SNPs on broad depression through the log of pack-years of cigarette smoking, adjusting for age, sex, current smoking status, and genetic ancestry (via principal components). In secondary analyses, we adjusted for age, sex, current smoking status, genetic ancestry (via principal components), income, education, and living status (urban vs. rural). In addition, we examined sex-stratified mediation models and sex-moderated mediation models. For both analyses, we adjusted for age, current smoking status, and genetic ancestry (via principal components). In the UK Biobank, rs6424532 [LOC105378800] had a statistically significant indirect effect on broad depression through the log of pack-years of cigarette smoking (p = 4.0 × 10-4) among all participants and a marginally significant indirect effect among females (p = 0.02) and males (p = 4.0 × 10-3). Moreover, rs10501696 [GRM5] had a marginally significant indirect effect on broad depression through the log of pack-years of cigarette smoking (p = 0.01) among all participants and a significant indirect effect among females (p = 2.2 × 10-3). In the secondary analyses, the sex-moderated indirect effect was marginally significant for rs10501696 [GRM5] on broad depression through the log of pack-years of cigarette smoking (p = 0.01). In the COPDGene study, the effect of an SNP (rs10501696) in GRM5 on depressive symptoms and medication was mediated by log of pack-years (p = 0.02); however, no SNPs had a sex-moderated mediated effect on depressive symptoms. In the UK Biobank, we found SNPs in two genes [LOC105378800, GRM5] with an indirect effect on broad depression through the log of pack-years of cigarette smoking. In addition, the indirect effect for GRM5 on broad depression through smoking may be moderated by sex. These results suggest that genetic regions associated with broad depression may be mediated by cigarette smoking and this relationship may be moderated by sex.

Association of ADAM33 gene with COPD pathophysiology: a case–control study

BackgroundWorldwide, Chronic Obstructive pulmonary disease (COPD) is a main cause of morbidity and mortality. Considering the global increase in the prevalence of COPD, research on the genetic factors that predispose to COPD is reviving. Recently, ADAM 33 has been found to be related to severe lung function decline and COPD.Aim and objectiveThe present study is carried out with the main aim of determining the association of SNP, i.e., S2 (rs528557), with COPD.MethodA case–control methodology is used to recruit participants. 50 COPD patients over 40 years of age and with a history of more than 20 pack years of cigarette smoking were enlisted. The same number of age and gender-matched controls with no COPD history were involved. PCR sequencing was used to analyze the genetic polymorphism of the ADAM 33 gene (SNP, i.e., S2 (rs528557). Statistical analysis was carried out using SPSS version 21. The Chi-square test was used to determine the difference in SNP rs528557 genotypes and alleles between controls and COPD.ResultsThe findings of this study revealed that the G allele was present in all COPD cases (100%) and 72% of control (p = < 0.001). The minor C allele was 14% and 32% in COPD patients and control, respectively. The G/G genotype is overrepresented in cases (25.5%) than in the control (9.2%). The C/C genotype is overrepresented in controls (3.8%) than in COPD patients (0.9%).ConclusionThe findings of this study demonstrate a significant association of the ADAM 33 gene (SNP, i.e., S2 (rs528557) with COPD pathophysiology in the studied group.

Hypothetical Interventions on Diet Quality and Lifestyle Factors to Improve Breast Cancer Survival: The Pathways Study.

The number of breast cancer survivors is increasing, yet evidence to inform dietary and lifestyle guidelines is limited. This analysis included 3,658 participants from the Pathways Study, a prospective cohort of women diagnosed with invasive breast cancer. A healthy plant-based dietary index score (hPDI), an American Cancer Society (ACS) nutrition guidelines score, a 2015 Healthy Eating Index score (HEI), hours per week of moderate to vigorous physical activity (PA), and lifetime cumulative pack-years of cigarette smoking (SM) were each measured at diagnosis, 6, 24, and 72 months. Using g-computation, 5- and 10-year risk ratios (RR), risk differences, and 95% confidence intervals (CI) for all-cause mortality under hypothetical interventions on diet quality, PA, and SM, compared with the natural course (no intervention) were calculated. Hypothetical moderate to extreme interventions on hPDI, ACS, and HEI, each in combination with PA and SM, showed 11% to 56%, 9% to 38%, and 9% to 49% decreases in 5-year risks of all-cause mortality compared with no intervention, respectively [(hPDI: RRmoderate = 0.89, 95% CI: 0.82-0.94; RRextreme = 0.44, 95% CI: 0.26-0.67), (ACS: RRmoderate = 0.91, 95% CI: 0.85-0.96; RRextreme = 0.62, 95% CI: 0.43-0.82), (HEI: RRmoderate = 0.91, 95% CI: 0.84-0.95; RRextreme = 0.51, 95% CI: 0.33-0.72)]. While 10-year relative risks were slightly attenuated, absolute risk reductions were more pronounced. Interventions to improve diet quality, increase PA, or reduce SM at the time of diagnosis may improve survival among breast cancer survivors. We estimate that over 10% of deaths could be delayed by even moderate adoption of these behaviors.

Smoking Intensity Increases Diaphragm Muscle Injury: A Clinicopathologic Study.

Studying the effects of smoking intensity is important to evaluate the risk of tobacco use on a range of illnesses, such as as sarcopenia among the elderly. Thus, this study aimed to analyze the effects of pack-years of cigarette smoking on the diaphragm muscle (DIAm) histopathology of postmortem samples. Subjects were divided into three groups: never-smoker (n = 46); less than 30 pack-years of smoking (n = 12); and more than 30 pack-years of smoking (n = 30). Diaphragm samples were stained with Picrosirius red and hematoxylin and eosin stain for general structure. Participants with more than 30 pack-years of cigarette smoking had a significant increase in adipocytes, blood vessels and collagen deposit, as well as an increase in histopathological alterations. Pack-years of smoking was associated with DIAm injury. However, further clinicopathological studies are needed to confirm our findings.

Cannabis smoking, tobacco cigarette smoking, and adenomyosis risk

To investigate cannabis smoking and tobacco cigarette smoking in relation to adenomyosis risk. We used data from a case-control study of adenomyosis conducted among enrollees ages 18-59 years of an integrated health care system in Washington State. The case-control study used 2 control groups given the challenge of selecting noncases when cases are diagnosed by hysterectomy. Cases (n = 386) were enrollees with incident, pathology-confirmed adenomyosis diagnosed between April 1, 2001, and March 31, 2006. The 2 control groups comprised hysterectomy controls (n = 233) with pathology-confirmed absence of adenomyosis and population controls (n = 323) with an intact uterus selected randomly from the health care system population and frequency matched to cases on age. Detailed data on cannabis and tobacco cigarette smoking history were ascertained through in-person structured interviews, allowing estimation of joint-years of cannabis smoking and pack-years of tobacco cigarette smoking. Odds ratios (ORs) and 95% confidence intervals (CIs) for the associations between cannabis smoking, tobacco cigarette smoking, and adenomyosis were estimated using multivariable unconditional logistic regression. Analyses were adjusted for age, reference year, menarche age, education, and pack-years of cigarette smoking (or joint-years of cannabis smoking). No association was observed between cannabis smoking history and adenomyosis risk. However, we did observe the suggestion of an association between ever tobacco cigarette smoking and adenomyosis risk, comparing cases to hysterectomy controls (OR, 1.3; 95% CI, 0.9-1.9) and population controls (OR, 1.2; 95% CI, 0.8-1.8). Our data suggested a 50% increased odds of adenomyosis with >15 pack-years of smoking (vs. never smoking), comparing cases to hysterectomy controls (OR, 1.5; 95% CI, 0.9-2.6; Ptrend=.135). The suggestion of a 40% increased adenomyosis odds was observed with smoking >5-15 pack-years (vs. never smoking), comparing cases to population controls (OR, 1.4; 95% CI, 0.8-2.4; Ptrend=0.136). In the first study of cannabis smoking and adenomyosis risk, no association was observed. However, our data suggested an increased odds of adenomyosis with history of tobacco cigarette smoking. Further research is warranted to replicate our results given the substantial morbidity with adenomyosis and frequency of cigarette smoking and recreational and medical cannabis use.

Association of Pack-Years of Cigarette Smoking With Survival and Tumor Progression Among Patients Treated With Chemoradiation for Head and Neck Cancer

After 10 pack-years of smoking was initially established as a threshold for risk stratification, subsequent clinical trials incorporated it to identify candidates for treatment deintensification. However, several recent studies were unable to validate this threshold externally, and the threshold for smoking exposure remains unclear. To estimate the threshold of pack-years of smoking associated with survival and tumor recurrence among patients with head and neck cancer. This single-institution, cohort study included patients with nonmetastatic head and neck cancer receiving chemoradiation from January 2005 to April 2021. Data were analyzed from January to April 2022. Heavy vs light smoking using 22 pack-years as a threshold based on maximizing log-rank test statistic. Overall survival (OS), progression-free survival (PFS), locoregional failure (LRF), and distant failure (DF). A total of 518 patients (427 male [82.4%]; median [IQR] age, 61 [55-66] years) were included. Median (IQR) follow-up was 44.1 (22.3-72.8) months. A nonlinear Cox regression model using restricted cubic splines showed continuous worsening of OS and PFS outcomes as pack-years of smoking increased. The threshold of pack-years to estimate OS and PFS was 22. Cox multivariable analysis (MVA) showed that more than 22 pack-years was associated with worse OS (adjusted hazard ratio [aHR] 1.57; 95% CI, 1.11-2.22; P = .01) and PFS (aHR, 1.38; 95% CI, 1.00-1.89; P = .048). On Fine-Gray MVA, heavy smokers were associated with DF (aHR, 1.71; 95% CI, 1.02-2.88; P = .04), but not LRF (aHR, 1.07; 95% CI, 0.61-1.87; P = .82). When 10 pack-years of smoking were used as a threshold, there was no association for OS (aHR, 1.23; 95% CI, 0.83-1.81; P = .30), PFS (aHR, 1.11; 95% CI, 0.78-1.57; P = .56), LRF (aHR, 1.19; 95% CI, 0.64-2.21; P = .58), and DF (aHR, 1.45; 95% CI, 0.82-2.56; P = .20). Current smoking was associated with worse OS and PFS only among human papillomavirus (HPV)-positive tumors (OS: aHR, 2.81; 95% CI, 1.26-6.29; P = .01; PFS: aHR, 2.51; 95% CI, 1.22-5.14; P = .01). In this cohort study of patients treated with definitive chemoradiation, 22 pack-years of smoking was associated with survival and distant metastasis outcomes. Current smoking status was associated with adverse outcomes only among patients with HPV-associated head and neck cancer.

Smoking Behaviors and Prognosis in Patients With Non–Muscle-Invasive Bladder Cancer in the Be-Well Study

Tobacco smoking is an established risk factor associated with bladder cancer, yet its impact on bladder cancer prognosis is unclear. To examine associations of use of tobacco (cigarettes, pipes, and cigars), e-cigarettes, and marijuana with risk of recurrence and progression of non-muscle-invasive bladder cancer (NMIBC) and to explore use of smoking cessation interventions. The Be-Well Study is a prospective cohort study of patients with NMIBC diagnosed from 2015 to 2019 and followed-up for 26.4 months in the Kaiser Permanente Northern and Southern California integrated health care system. Eligibility criteria were age at least 21 years, first NMIBC diagnosis (stages Ta, Tis, or T1), alive, and not in hospice care. Exclusion criteria were previous diagnosis of bladder cancer or other cancer diagnoses within 1 year prior to or concurrent with NMIBC diagnosis. Data were analyzed from April 1 to October 4, 2022. Use of cigarettes, pipes, cigars, e-cigarettes, and marijuana was reported in the baseline interview. Use of smoking cessation interventions (counseling and medications) was derived from electronic health records. Hazard ratios (HRs) and 95% CIs of recurrence and progression of bladder cancer were estimated by multivariable Cox proportional hazards regression. A total of 1472 patients (mean [SD] age at diagnosis, 70.2 [10.8%] years; 1129 [76.7%] male patients) with NMIBC were enrolled at a mean (SD) of 2.3 (1.3) months after diagnosis, including 874 patients (59.4%) who were former smokers and 111 patients (7.5%) who were current cigarette smokers; 67 patients (13.7%) smoked pipes and/or cigars only, 65 patients (4.4%) used e-cigarettes, 363 patients (24.7%) used marijuana. Longer cigarette smoking duration and more pack-years were associated with higher risk of recurrence in a dose-dependent manner, with the highest risks for patients who had smoked for 40 or more years (HR, 2.36; 95% CI, 1.43-3.91) or 40 or more pack-years (HR, 1.97; 95% CI, 1.32-2.95). There was no association of having ever smoked, being a former or current cigarette smoker, and years since quit smoking with recurrence risk. No associations with pipes, cigars, e-cigarettes, or marijuana were found. Of 102 patients offered a smoking cessation intervention, 57 (53.8%) received an interventions after diagnosis, with female patients more likely than male patients to engage in such interventions (23 of 30 female patients [76.7%] vs 34 of 76 male patients [44.7%]; P = .003). These findings suggest that longer duration and more pack-years of cigarette smoking were associated with higher risk of NMIBC recurrence. Cigarette smoking remains a critical exposure before and after diagnosis in survivors of NMIBC.

ODP048 Large Bilateral Adrenal Lesions Abutting Right Hemidiaphragm in a Man from Texas

Abstract Sporadic cases of disseminated histoplasmosis (DHI) have been reported in several regions of the US, mainly inimmunocompromised patients where involvement of the adrenal gland, either unilaterally or bilaterally, is often being the only demonstrable site of active fungal disease in the setting of nonspecific clinical complaints. While DHI is not immediately life-threatening, adrenal involvement might be the most concerning complications due to potential risk of the gland destruction by the expanding infection or its treatment; it is considered that adrenal insufficiency is one of the most common causes of death in patients with DHI. We present a case of 78-year-old immunocompetent gentleman with history of hypertension, ischemic heart disease, atrial fibrillation and 30 pack-years of cigarette smoking who presented with low-grade fever, anorexia and 30 lbs weight loss. As a part of diagnostic evaluation, CT abdomen was performed and bilateral adrenal lesions were reported: right adrenal mass measured 4.6×3.4 cm, and the left adrenal mass 4.1×3.2 cm in maximal axial dimensions. Of note, the right adrenal mass abutted the crus of the right hemidiaphragm and undersurface of the liver. Hormonal evaluation was performed and did not show any excess secretions. GI consult was called for evaluation of adrenal gland access and biopsy: endoscopic ultrasound guided FNA biopsy access was performed and revealed findings compatible with adrenal histoplasmosis and no malignant cells. ID consult was sought: evaluation and prompt start of antifungal therapy were undertaken: IV Amphotericin B, followed by oral Itraconazole for total of 12 months. Patient has remained stable during initial evaluation: due to his age and comorbid conditions, he was admitted to the hospital during which Cosyntropin stimulation test was performed: results have revealed 12.9 at baseline and 17.6 after stimulation. Interdisciplinary discussion was held and resulted in decision to start steroid replacement therapy due to rather mild response to stimulation and significant risk of collateral damage to the remaining adrenal tissue during the antifungal therapy. Patient has responded to therapy well, though had some worsening of his cardiac function which required optimization of diuretic therapy. Patient's vital signs have remained stable, he has reported improved appetite and started to regain some of the lost weight; his electrolytes remained stable. Six-month interval imaging has shown reduction of the size of the adrenal gland sizes and no evidence of gland hemorrhage; notably, adrenal gland improvement has generally paralleled imaging improvement in other involved organs. Steroid therapy is being continued for total of 12 months. DHI still remains a serious problem in certain regions of the US and the world and has to remain an essential part of the differential diagnosis of the adrenal lesions allowing earlier treatment, gland preservation and avoidance of life-threatening complications. Presentation: No date and time listed

Ordinal scoring of coronary artery calcification in low dose computed tomography is predictive factor of all-cause death and cardiovascular events

Abstract Background Lung cancer and cardiovascular disease (CVD) are leading worldwide mortality causes firmly related to smoking. Lung cancer screening (LCS) consisted in performing low-dose computed tomography (LDCT) offers an opportunity for simultaneous coronary artery calcification (CAC) assessment. Purpose The study aimed to determine the usefulness of the visual assessment of CAC in the prediction of all-cause death and non-fatal cardiovascular outcomes including myocardial infarction and stroke. Methods The study involved 6580 participants aged 50–79 years, current or former smokers with a cigarette smoking history of at least 30 pack-years, who were qualified for lung cancer screening program performed between April 2016 and May 2018. CAC was visually scored on ungated LDCT scans in the range of 0–12 based on the length of calcification involvement in four main coronary arteries. CAC severity was categorized into groups of 0, 1–3, 4–12. The primary outcome was all-cause mortality. The secondary outcome was major adverse cardiovascular events (composite of CVD death, nonfatal myocardiaI infarction, nonfatal stroke). The outcomes data were obtained by using the National Health Care Provider Registry of death and hospitalizations. The mean time of follow-up was 41.1 months (SD 8.3). Logistic regression analysis was used to determine the risk of mortality according to the CAC category adjusted for age, pack-years of cigarette smoking, and sex. Results The rate of all-cause death substantially increased in groups of higher CAC and it was consecutively 2.7% (89 of 3288 subjects) for a score of 0, 4.2% (66 of 1582 subjects) for a score of 1–3 and 8.3% (145 of 1742 subjects) for a score of 4–12. With the use of subjects with a CAC score of 0 as the reference group, adjusted for sex, age, and pack-years of smoking, a CAC score of at least 4 was a significant predictor of all-cause death (hazard ratio [HR], 1.89; 95% CI: 1.42; 2.52; P&amp;lt;0.05). Similar results were observed for the composite of CVD death, nonfatal myocardial infarction, nonfatal stroke with even greater significance. The rate of secondary outcames was 1.6% (51/3276) in a 0 score cohort, 3.0% (47/1570) in a 1–3 score cohort and 7.5% (130/1732) in a 4–12 score cohort. Both CAC score in the range 1–3 ([HR], 1.57; 95% CI: 1.05; 1.2.35; P&amp;lt;0.05), and 4–12 ([HR], 3.55; 95% CI: 2.50; 5.04; P&amp;lt;0.05) were a significant predictors of major adverse cardiovascular event incidence. Conclusions Visual assessment of CAC provides solid evidence of all-cause death and cardiovascular incidents independently of traditional coronary risk factors. Therefore evaluation of CAC in LDCT scans offers a unique opportunity for instituting CVD risk assessment in lung cancer screening program. Funding Acknowledgement Type of funding sources: Public grant(s) – National budget only. Main funding source(s): National Centre for Research and Development of Poland.

Causal analysis identifies small HDL particles and physical activity as key determinants of longevity of older adults.

SummaryBackgroundThe hard endpoint of death is one of the most significant outcomes in both clinical practice and research settings. Our goal was to discover direct causes of longevity from medically accessible data.MethodsUsing a framework that combines local causal discovery algorithms with discovery of maximally predictive and compact feature sets (the “Markov boundaries” of the response) and equivalence classes, we examined 186 variables and their relationships with survival over 27 years in 1507 participants, aged ≥71 years, of the longitudinal, community-based D-EPESE study.FindingsAs few as 8-15 variables predicted longevity at 2-, 5- and 10-years with predictive performance (area under receiver operator characteristic curve) of 0·76 (95% CIs 0·69, 0·83), 0·76 (0·72, 0·81) and 0·66 (0·61, 0·71), respectively. Numbers of small high-density lipoprotein particles, younger age, and fewer pack years of cigarette smoking were the strongest determinants of longevity at 2-, 5- and 10-years, respectively. Physical function was a prominent predictor of longevity at all time horizons. Age and cognitive function contributed to predictions at 5 and 10 years. Age was not among the local 2-year prediction variables (although significant in univariable analysis), thus establishing that age is not a direct cause of 2-year longevity in the context of measured factors in our data that determine longevity.InterpretationThe discoveries in this study proceed from causal data science analyses of deep clinical and molecular phenotyping data in a community-based cohort of older adults with known lifespan.FundingNIH/NIA R01AG054840, R01AG12765, and P30-AG028716, NIH/NIA Contract N01-AG-12102 and NCRR 1UL1TR002494-01.

Opium use and risk of bladder cancer: a multi-centre case-referent study in Iran.

BackgroundBladder cancer (BC) is the 10th most common type of cancer worldwide and the fourth most common type of cancer in Iran. Opium use is considered as one of the risk factors for BC. We aim to assess the association between various parameters of opium use, which in Iran is mainly ingested or smoked in various forms, and the risk of BC.MethodIn this multi-centre case-referent study in Iran, 717 BC cases and 3477 referents were recruited to the study from May 2017 until July 2020. Detailed histories of opium use (duration, amount, frequency) and potential confounders were collected by trained interviewers. Multivariable unconditional logistic regression models were used to measure adjusted odds ratio (OR) and 95% confidence intervals (CI). The ORs were adjusted for age, gender, place of residence and pack-years of cigarette smoking.ResultsRegular opium consumption was associated with an increased risk of BC (OR 3.5, 95% CI: 2.8, 4.3) compared with subjects who never used opium. Compared with continuous users, the risk decreased to one-third for those who stopped opium more than 10 years ago. The adjusted OR for those who used both crude opium (teriak) and opium juice was 7.4 (95% CI: 4.1, 13.3). There was a joint effect of opium and tobacco (OR for users of both opium and tobacco 7.7, 95% CI: 6.0, 9.7).ConclusionsRegular opium use is associated with an approximately 4-fold risk for BC. The OR decreases along with the increasing time since stopping opium use.

Marijuana smoking and cataract

Cigarette smoking is a well-known risk factor for cataract and other ailments, including heart disease, lung cancer, and chronic obstructive pulmonary disease. Cannabis smoke, like tobacco smoke, contains a comparable variety of carcinogenic and toxic compounds. In the present study, we analyzed UK Biobank data to determine whether smoking cannabis, like cigarettes, might be related to cataract. Our analysis included all UK Biobank subjects with cataracts and information on cannabis and cigarette smoking habits. The diagnosis of cataract was ascertained using the 10th Revision of the International Classification of Diseases (ICD10), H25. The age at diagnosis of cataract was obtained from UK Biobank data field 4700. Cannabis information was recorded in UK Biobank category 143, data field 20453, ever taken cannabis. Subjects who used cannabis 11-100 times or more were significantly younger (4-5 years) when they developed cataract than subjects who never used cannabis. To determine the relationship of current cigarette smoking to cannabis use and age at cataract, the univariate general linear model of SPSS was used, dependent variable age at cataract, fixed factor cannabis use, random factor pack years of cigarettes smoked. Cannabis use was significantly related to age at cataract diagnosis (P<0.001) and independent of the effect of pack-years of cigarettes smoked (P=0.008). Linear regression revealed an insignificant relationship between pack-years of cigarette smoking and age at cataract diagnosis (P=0.073). To further evaluate the relationship of cannabis to cataract, propensity score matching was performed. We identified 28,432 subjects with cataract. Current cigarette smoking and age were covariates;cannabis use (yes/no) was the indicator variable.Current cigarette smoking was significantly associated with a 1.2 odds ratio for cataract. Cannabis use was not significantly associated with the odds ratio for cataract. Like tobacco smoke, cannabis smoke contains thousands of organic and inorganic chemical compounds. Cannabis tar is chemically similar to tar found in tobacco smoke, and over fifty known carcinogens have been identified in cannabis smoke, including nitrosamines, reactive aldehydes, and polycyclic hydrocarbons. Thus, the association of cannabis with cataract that we report here is not entirely surprising. Further studies are warranted.

A Nested Case-Control Study of Lung Cancer for Immune Biomarkers

<h3>Purpose/Objective(s)</h3> Smoking is the leading cause of lung cancer, which is the leading cause of cancer mortality worldwide, with 1.2 million deaths a year. Lung cancer has a very poor prognosis; over half of people diagnosed die within one year of diagnosis and the 5-year survival is less than 18%. Prior to cancer development, smokers develop multiple lung problems associated with chronic inflammation, which can promote progression to cancer. The aim of the study was to examine if immune competence would enhance or reduce the risk of lung cancer development among high-risk smokers. The hypothesis is that smokers who developed lung cancer would have a higher frequency of chronic inflammation induced myeloid-derived suppressor cells (MDSC) and/or regulatory T cells (Treg), three years or more prior to lung cancer diagnosis (baseline), compared to smokers who remained cancer-free. Additionally, smokers who developed cancer would have higher levels of certain inflammatory cytokines at baseline. <h3>Materials/Methods</h3> A case-control study of incident lung cancer was conducted within the participants of the Pittsburgh Lung Screening Study (PLuSS), a longitudinal low-dose CT screening study for early detection of lung cancer among smokers with a history of heavy smoking (median 47 pack-years of cigarette smoking). Cases consisted of 40 current or former smokers who developed lung cancer during follow-up after repeated blood draws and the control group consisted of 40 PLuSS participants, free of cancer, who were individually matched to the index case by age, sex, smoking status, and year of blood draw. Live peripheral blood mononuclear cells (PBMC) were thawed and analyzed for MDSC, CD4 T cells, and Treg by flow cytometry. Cytokines and chemokines were quantified in two repeated serum samples per subject using the next generation multiplex immunoassays. <h3>Results</h3> There was no statistically significant difference in overall MDSC percentage of PBMC nor in subtypes (PMN-MDSC, M-MDSC and e-MDSC) between cases and controls. There was also no difference found for Tregs. However, CD4 T cells were elevated in lung cancer cases and were associated with an increased risk of lung cancer overall (odds ratio [OR] = 2.61, 95% confidence interval [CI] = 0.73-9.32, p trend = 0.1409). Lung cancer cases had significantly higher levels of serum inflammatory cytokines IL-17A and Il-12/IL-23p40 at both early (median 84 months) and late time points (7 months prior to cancer diagnosis) (all <i>P</i>s < 0.05). <h3>Conclusion</h3> Lung cancer cases are associated with elevated levels of CD4 T cells and pro-inflammatory cytokines, specifically IL-17A and IL-12/IL-23p40, as early as 7 years before cancer diagnosis. The study has the potential to identify immune cells and soluble factors that mediate lung cancer development in smokers and could be used as early biomarkers for risk assessment or early diagnosis of lung cancer.

COT-6 Body mass index and height in relation to brain tumor risk in a Japanese population

Purpose: Because the prognosis of the malignant brain tumor including glioblastoma is extremely worse than other cancer, it is important to clarify the preventive factors of the brain tumor in the prospective cohort study. In the Japanese epidemiologic study of the brain tumor, the report of the prospective cohort study has not been accomplished. Therefore, we have reported the study in recent years from a multipurpose cohort study (Japan Public Health Center-based Prospective Study: JPHC study) that the national cancer center was mainly conducted. This prospective study investigated the association between height and BMI (Body mass index) and brain tumor risk in an Asian population, whose distribution of anthropometric data differs from Westerners. Methods: A total of 106,324 subjects (50,438 men and 55,886 women) enrolled in JPHC Study, was followed from 1990. We divided participants into 5 categories based on the distribution of BMI as <18.5, 18.5- <23, 23- <25, 25- <27.5, and >-27.5 Kg/m2. We used the Cox proportional hazards regression model and estimated brain tumor incidence by gender and tumor subtype, with adjustment for potential confounding variables; age, sex, pack-years of cigarette smoking, alcohol intake, coffee intake, green tea intake, past history of allergy and past history of diabetes mellitus.Results: During an average follow-up of 18.1 years, 157 incident cases of brain tumor were newly identified, included glioma (n=60), meningioma (n =51), lymphoma(n=9), schwannoma(n=3), pituitary adenoma(n=2), and others(n=32). Higher BMI was significantly positively associated with the risk of brain tumor. This positive association of BMI was stronger in men and for meningioma in subgroup analyses. In contrast, height showed no clear association with brain tumor risk. Conclusion: Higher BMI was associated with an increased risk of brain tumor, in particular of meningioma, and among men.Full article has been published annals of epidemiology.

The Efficacy of Different Inflammatory Markers for the Prognosis of Patients with Malignant Tumors.

BackgroundInflammation is considered essential in cancer progression, as it affects the nutritional status and prognosis of patients. In this study, we aim to analyze the efficacy of various inflammatory markers in predicting prognosis in cancer patients.MethodsPatients with malignant tumor were included as primary and validation cohort. Basic clinical information, anthropometric indicators, body composition analysis, and serological indicators were recorded. After proposing the optimal thresholds by time-dependent receiver operating characteristic (ROC), univariate and multivariate Cox regression analyses were performed to analyze the association between inflammatory markers and overall survival (OS). A nomogram was established to develop a scored-inflammatory marker system. Eight inflammatory models based on combinations of inflammatory markers were assessed. Cox regression analysis was used to analyze the relationship of each inflammatory model and mortality of participants. Then, subanalysis of specific tumor types was conducted by Cox regression. Logistic regression models were used to analyze the relationship between different inflammatory models and malnutrition.ResultsUnivariate and multivariate Cox regression analyses indicated that pack-years of cigarette smoking, C-reactive protein (CRP), and systemic immune-inflammation index (SII) were related to the OS of cancer patients. A nomogram was constructed to develop a scored-inflammatory marker system. Among the eight inflammatory models, patients in model A had worst prognosis compared with patients in other models. Subanalysis next showed lung cancer, breast cancer and digestive system neoplasms patients in model A suffered the worst prognosis. Logistic regression indicated that model A was also with predictive value for malnutrition.ConclusionA scored-inflammatory marker system was established to predict the OS of cancer patients. The inflammatory models established in this study can be used to predict prognosis, as well as cancer-related malnutrition. Inflammatory model A suffered the worst OS and was with the predictive efficacy for malnutrition.

Illicit drug use and self-reported vision loss among military service members or veterans

IntroductionLittle is known about differences in vision loss prevalence among service members or veterans (SMVs) and civilians; further, no study has compared vision loss risk factors in these two populations....

Tobacco and marijuana use and their association with serum prostate-specific antigen levels among African American men in Chicago.

African American (AA) men experience more than twice the prostate cancer mortality as White men yet are under-represented in academic research involving prostate-specific antigen (PSA), a biomarker of prostate cancer aggressiveness. We examined the impact of self-reported tobacco (cigarette pack-years and current tobacco use including e-cigarettes) and current regular marijuana use on serum PSA level based on clinical laboratory testing among 928 AA men interviewed 2013-2018 in Chicago. We defined outcome of elevated PSA ≥ 4.0 ng/mL for logistic regression models and continuous PSA increases for general linear models. All models were adjusted for age, sociodemographic characteristics, healthcare utilization, body mass index, and self-reported health. Among 431 AA men age ≥ 55 years, we observed ∼ 5 times the odds of elevated PSA among those with > 1 pack-years of cigarette smoking vs. never-smokers (odds ratio [OR] = 5.09; 95% confidence interval [CI] = 1.57-16.6) and a quarter the odds of elevated PSA among current marijuana users vs. non-users (OR = 0.27; 95% CI = 0.08-0.96). PSA increased on average 1.20 ng/mL among other current tobacco users vs. non-users. Among older AA men, cigarette smoking history and current tobacco use were positively associated with an increase in PSA levels and current marijuana use were inversely associated with PSA levels. Future work with studies of diverse patient populations with cancer outcomes are needed to assess whether these behavioral characteristics contribute to racial/ ethnic disparities in prostate cancer outcomes. Our study provides novel evidence regarding potential differences in PSA levels among older AA men according to behavioral characteristics.

Mediterranean Diet Is Associated with Lower Breast Cancer Risk in the Framingham Offspring Cohort Study

Abstract Objectives We examined the prospective association between a Mediterranean diet pattern using four separate a priori indices of adherence and breast cancer risk in the Framingham Offspring (FOS) cohort. Methods The four indices included in this study reflect two different approaches to measuring adherence to a Mediterranean diet: a. scores based on population food intake distributions (i.e., the alternate Mediterranean Diet (aMED) and Mediterranean Diet (MDS) score); and b. scores based on recommended intakes of relevant foods (i.e., Mediterranean Style Dietary Pattern (MSDP) and Mediterranean Diet (MeDiet) scores). The scores were derived from a semi-quantitative food frequency questionnaire. Subjects included 1703 women, aged 30 years old and older, who were free of prevalent cancer. Each score was classified into three categories (low, moderate, and high) to evaluate the association between the Mediterranean diet and breast cancer risk (overall, post-menopausal, and hormone receptor positive) from 1991 through 2014. Cox proportional-hazards regression models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs), adjusting for confounding by age, physical activity, waist-to-height ratio, pack-years of cigarette smoking, supplement use, diabetes status, age at menopause and total calorie intake. Results During a median follow-up of approximately 18 years, 93 breast cancer cases were documented. Women in the highest category of MSDP score or MeDiet score had approximately 45% lower breast cancer risks than women in the lowest categories (MSDP high category HR:0.56, 95% CI: 0.33–0.94; MeDiet high category HR: 0.55, 95% CI: 0.31–0.98). This effect was similar for post-menopausal breast cancer cases. In addition, the high (vs. low) MeDiet score was associated with 55% decreased risk of hormone receptor positive breast cancer (HR:0.45, 95% CI:0.23–0.87). Neither of the scores calculated on the basis of dietary intakes in the study population (i.e., aMED, MDS) was associated with breast cancer risk. Conclusions In this large prospective cohort, scores based on recommended intakes of relevant Mediterranean diet foods may lead to strong evidence of the inverse relation between a Mediterranean dietary pattern and incidence of breast cancer among women aged 30 years old or older in the US. Funding Sources The Framingham Heart Study.

Retrospective assessment of Lung-RADS® performance in the Silesian Lung Cancer Screening Pilot Study

Background. A high percentage of false positive results, observed in lung cancer screening studies with low-dose computed tomography (LDCT), caused the modification of radiological assessment methods. According to the International Early Lung Cancer Action Program (IELCAP) all non-calcified nodules with a dimension ≥ 4 mm were considered as positive. Implementation of classification the Lung CT screening Reporting and Data System (Lung-RADS®) recommends additional testing only for nodules ≥ 6 mm, which reduced of false positive results. Methods. We provided a retrospective analysis of 601 LDCT scans, in asymptomatic volunteers of Pilot Silesian Study of Early Lung Cancer Detection, with at least 20 pack-years of cigarette smoking. The analysis of non- and invasive interventions was done. Assessment of nodules according to the Lung-RADS® system was done. Then the percentage of interventions that could be avoided using the Lung-RADS® criteria was estimated. Results. In total, 1016 nodules were identified in 265 participants. The positive result of screening was defined as a presence of solid or part-solid nodule ≥ 5 mm and ≥ 8 mm in the case of a nonsolid nodule in line with the IELCAP protocol. Screening based on the IELCAP protocol resulted in 200 positive results and based on Lung-RADS® in the 116 positives. The frequency of lung cancers among participants with a positive result was 7 of 200 (4.0%) (95% CI: 1.0%, 6.0%) for IELCAP and 7 of 116 (6.0%) (95% CI: 2.7%, 9.3%) for Lung-RADS®. The Lung-RADS® criteria reduced number of non- and invasive procedures by 48.8% and 24.1%, compared to IELCAP protocol. Conclusions. Adopting the Lung-RADS® classification system may reduce harms and improve the efficiency of lung cancer screening programs.