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2.
BMJ Open Respir Res ; 11(1)2024 May 07.
Article in English | MEDLINE | ID: mdl-38719502

ABSTRACT

INTRODUCTION: The COVID-19 pandemic continues to be a global threat to public health, with over 766 million confirmed cases and more than 6 million reported deaths. Patients with a smoking history are at a greater risk of severe respiratory complications and death due to COVID-19. This study investigated the association between smoking history and adverse clinical outcomes among COVID-19 patients admitted to a designated medical centre in Saudi Arabia. METHODS: A retrospective observational cohort study was conducted using patient chart review data from a large tertiary medical centre in the eastern region of the country. Patients admitted between January and December 2020 were screened. The inclusion criteria were ≥18 years of age and confirmed COVID-19 infection via reverse-transcription-PCR. The exclusion criteria were unconfirmed COVID-19 infection, non-COVID-19 admissions, unconfirmed smoking status, vaccinated individuals, essential chart information missing or refusal to consent. Statistical analyses comprised crude estimates, matching weights (as the main analysis) and directed acyclic graphs (DAGs) causal pathway analysis using an ordinal regression model. RESULTS: The sample comprised 447 patients (never-smoker=321; ever-smoker=126). The median age (IQR) was 50 years (39-58), and 73.4% of the sample were males. A matching weights procedure was employed to ensure covariate balance. The analysis revealed that the odds of developing severe COVID-19 were higher in the ever-smoker group with an OR of 1.44 (95% CI 0.90 to 2.32, p=0.130). This was primarily due to an increase in non-invasive oxygen therapy with an OR of 1.05 (95% CI 0.99 to 1.10, p=0.101). The findings were consistent across the different analytical methods employed, including crude estimates and DAGs causal pathway analysis. CONCLUSION: Our findings suggest that smoking may increase the risk of adverse COVID-19 outcomes. However, the study was limited by its retrospective design and small sample size. Further research is therefore needed to confirm the findings.


Subject(s)
COVID-19 , Propensity Score , SARS-CoV-2 , Humans , COVID-19/epidemiology , Male , Retrospective Studies , Middle Aged , Female , Saudi Arabia/epidemiology , Adult , Severity of Illness Index , Tobacco Smoking/epidemiology , Tobacco Smoking/adverse effects , Aged , Risk Factors , Hospitalization/statistics & numerical data
3.
BMC Cardiovasc Disord ; 24(1): 290, 2024 Jun 01.
Article in English | MEDLINE | ID: mdl-38822250

ABSTRACT

BACKGROUND: Little is known about patient profile changes in medical facilities in our country, leading to this study to describe and compare patient profiles in 2010 and 2022. PATIENTS AND METHODS: This was a cross-sectional study with new outpatients aged 15 years and more seen in the cardiology department of the UH-GT. Measurements included height, weight and body mass index (BMI). Systolic blood pressure (SBP) and diastolic blood pressure (DBP) were recorded. Quantitative data are presented as the mean with standard deviation, and categorical one as proportions. Statistical tests were the t test to compare means and chi-test for categorical variables. The level of significance was set to 0.05. RESULTS: The sample consisted of 515 new patients (199 in 2010 and 316 in 2022) with 59.1% female in 2010 and 60.1% in 2022 (p = 0.821). We noticed an increase in hypertension (59.1-71.8%, p = 0.003) and a decrease in tobacco smoking (from 13 to 05.4%, p = 0.002) and stroke (from 05.8 to 02.2%, p = 0.033). Height increased significantly from 1.59 m to 1.66 m, p = 0.002. SBP and DBP showed significant decreases in their means from 155.43 to 144.97 mmHg, p = < 0.001 for SBP and from 95.53 to 89.02 mmHg, p = < 0.001 for DBP. CONCLUSIONS: Cardiovascular risk factors showed different trends with decreasing tobacco smoking, similar to systolic and diastolic blood pressure, albeit with an increase in hypertension prevalence. Other CVrf values increased. Awareness campaigns must be reinforced and maintained to obtain their decrease.


Subject(s)
Blood Pressure , Cardiology Service, Hospital , Hospitals, University , Hypertension , Humans , Cross-Sectional Studies , Female , Male , Middle Aged , Adult , Aged , Hypertension/diagnosis , Hypertension/physiopathology , Hypertension/epidemiology , Time Factors , Risk Factors , Young Adult , Tobacco Smoking/adverse effects , Tobacco Smoking/epidemiology , Prevalence , Stroke/epidemiology , Stroke/diagnosis , Adolescent , Cardiovascular Diseases/epidemiology , Cardiovascular Diseases/diagnosis , Cardiovascular Diseases/physiopathology , Risk Assessment
4.
Nature ; 629(8013): 910-918, 2024 May.
Article in English | MEDLINE | ID: mdl-38693263

ABSTRACT

International differences in the incidence of many cancer types indicate the existence of carcinogen exposures that have not yet been identified by conventional epidemiology make a substantial contribution to cancer burden1. In clear cell renal cell carcinoma, obesity, hypertension and tobacco smoking are risk factors, but they do not explain the geographical variation in its incidence2. Underlying causes can be inferred by sequencing the genomes of cancers from populations with different incidence rates and detecting differences in patterns of somatic mutations. Here we sequenced 962 clear cell renal cell carcinomas from 11 countries with varying incidence. The somatic mutation profiles differed between countries. In Romania, Serbia and Thailand, mutational signatures characteristic of aristolochic acid compounds were present in most cases, but these were rare elsewhere. In Japan, a mutational signature of unknown cause was found in more than 70% of cases but in less than 2% elsewhere. A further mutational signature of unknown cause was ubiquitous but exhibited higher mutation loads in countries with higher incidence rates of kidney cancer. Known signatures of tobacco smoking correlated with tobacco consumption, but no signature was associated with obesity or hypertension, suggesting that non-mutagenic mechanisms of action underlie these risk factors. The results of this study indicate the existence of multiple, geographically variable, mutagenic exposures that potentially affect tens of millions of people and illustrate the opportunities for new insights into cancer causation through large-scale global cancer genomics.


Subject(s)
Carcinoma, Renal Cell , Environmental Exposure , Geography , Kidney Neoplasms , Mutagens , Mutation , Female , Humans , Male , Aristolochic Acids/adverse effects , Carcinoma, Renal Cell/genetics , Carcinoma, Renal Cell/epidemiology , Carcinoma, Renal Cell/chemically induced , Environmental Exposure/adverse effects , Environmental Exposure/analysis , Genome, Human/genetics , Genomics , Hypertension/epidemiology , Incidence , Japan/epidemiology , Kidney Neoplasms/genetics , Kidney Neoplasms/epidemiology , Kidney Neoplasms/chemically induced , Mutagens/adverse effects , Obesity/epidemiology , Risk Factors , Romania/epidemiology , Serbia/epidemiology , Thailand/epidemiology , Tobacco Smoking/adverse effects , Tobacco Smoking/genetics
5.
Sci Rep ; 14(1): 8550, 2024 04 12.
Article in English | MEDLINE | ID: mdl-38609449

ABSTRACT

Smoking may increase the risk of diabetic foot disease and ulceration. It does so by impairing glycaemic control and promoting the formation of advanced glycated end-products. Additionally, smoking is known to delay surgical wound healing and accelerate peripheral arterial disease. We aimed to determine whether toe pressures differed in smokers with a foot ulcer, when compared to non-smokers and ex-smokers, as well as ulcer outcomes at 12 months, among patients attending Blacktown Hospital High Risk Foot Service (HRFS). This study is a retrospective analysis of our prospectively collected clinic database. Eligible participants were adults attending the HRFS between June 2020 and April 2022. Participants were included if they had an ulcer, at least one systolic toe pressure reading completed at their initial visit and attended at least one follow-up visit. Participants were followed until healing, loss to follow-up or a minimum of 12 months. A total of 195 participants were included; 36 smokers, 82 ex-smokers, and 77 controls who had never smoked. Smoking status was by self-report. Current smokers were significantly younger at initial presentation (p = .002) and tended towards lower socioeconomic status (p = .067). Current smokers were significantly more likely to have ischaemic grade 3 toe pressures (< 30 mmHg) of their left foot (p = .027), suggestive of reduced perfusion. At the end of follow up period, smokers had the numerically highest rates of minor amputations. In conclusion, smokers ulcerate younger and are more likely to have grade 3 ischaemia. Collecting information about the brachial artery pressures and the time since the last cigarette may clarify any relationship between smoking and toe pressures.Trial registration: WSLHD HREC ethics approval 2111-02 and ANZCTR registration 382470. Registered on 15/09/2021.


Subject(s)
Foot Diseases , Ulcer , Adult , Humans , Retrospective Studies , Tobacco Smoking/adverse effects , Smokers , Toes
6.
JMIR Res Protoc ; 13: e54041, 2024 04 24.
Article in English | MEDLINE | ID: mdl-38657239

ABSTRACT

BACKGROUND: In the last few years, several nicotine products have become available as alternatives to smoking tobacco. While laboratory and limited clinical studies suggest that these devices are less toxic compared to classic tobacco cigarettes, very little is known about their epidemiological impact. Visiting the emergency department (ED) often represents the first or even the only contact of patients with the health care system. Therefore, a study conducted at the ED to assess the impact of these products on health can be reliable and reflect a real-life setting. OBJECTIVE: The aim of this noninterventional observational study (SMOPHED study) is to analyze the association between the severity of clinical presentation observed during ED visits among patients using various nicotine products and the subsequent outcomes, specifically hospitalization and mortality. METHODS: Outcomes (hospitalization and mortality in the ED) will be examined in relation to various patterns of nicotine products use. We plan to enroll approximately 2000 participants during triage at the ED. These individuals will be characterized based on their patterns of tobacco and nicotine consumption, identified through a specific questionnaire. This categorization will allow for a detailed analysis of how different usage patterns of nicotine products correlate with the clinical diagnosis made during the ED visits and the consequent outcomes. RESULTS: Enrollment into the study started in March 2024. We enrolled a total of 901 participants in 1 month (approximately 300 potential participants did not provide the informed consent to participate). The data will be analyzed by a statistician as soon as the database is completed. Full data will be published by December 2024. CONCLUSIONS: There is substantial debate about the harm reduction potential of alternative nicotine products in terms of their smoking-cessation and risk-reduction potential. This study represents an opportunity to document epidemiological data on the link between the use of different types of nicotine products and disease diagnosis and severity during an ED visit, and thus evaluate the harm reduction potential claims for these products. INTERNATIONAL REGISTERED REPORT IDENTIFIER (IRRID): PRR1-10.2196/54041.


Subject(s)
Emergency Service, Hospital , Adult , Female , Humans , Male , Middle Aged , Emergency Service, Hospital/statistics & numerical data , Hospitalization/statistics & numerical data , Nicotine/adverse effects , Observational Studies as Topic , Phenotype , Severity of Illness Index , Tobacco Smoking/epidemiology , Tobacco Smoking/adverse effects
8.
Foot Ankle Surg ; 30(4): 343-348, 2024 Jun.
Article in English | MEDLINE | ID: mdl-38368158

ABSTRACT

INTRODUCTION: Tobacco smoking is linked to an elevated risk of osteomyelitis and delayed healing in long bone fractures. However, the impact of smoking on bone union and soft tissue recovery following ankle fractures remains unclear. This study presents a retrospective comparative analysis evaluating the effects of chronic heavy tobacco smoking on the healing process and outcomes of ankle fractures after surgical interventions. MATERIALS AND METHODS: We examined 220 consecutive cases of chronic heavy smokers (CHS) with closed ankle fractures who were referred to our unit for further treatment. A control group, consisting of 220 age- and sex-matched individuals (non-smokers with closed ankle fractures), was identified for comparative analysis. We collected clinical data, including pre-existing comorbidities, Lauge-Hansen fracture classification, necessity for surgery, and the surgical procedures performed. The primary outcomes investigated were the time required for fracture union and wound healing. Secondary outcomes included postoperative complications such as prolonged pain, bleeding, swelling, infection, compartment syndrome, and neurovascular impairment, as well as the incidence of delayed union, non-union, and the need for further intervention. Both cohorts were monitored for a minimum of 24 months. RESULTS: Our analysis revealed that the surgical cohort of chronic heavy smokers exhibited a statistically significant delay in fracture union compared to both the conservatively managed smokers and the control group. Further scrutiny of the surgical cohort of chronic smokers indicated a significant correlation between smoking and extended postoperative pain duration, persistent swelling at the fracture site, and both superficial and deep wound infections. Additionally, these patients experienced delays in both fracture union and wound healing when compared to the control group. Similarly, the conservatively managed chronic smokers showed a marginal increase in the incidence of post-injury pain duration, extended swelling at the fracture site, and delayed union compared to the control group. CONCLUSION: Patients who are chronic heavy smokers and require surgical intervention for ankle fractures should be made aware of their increased risk for delayed fracture union and poor wound healing. Orthopedic surgeons should proactively encourage these patients to participate in smoking cessation programs.


Subject(s)
Ankle Fractures , Fracture Healing , Humans , Male , Female , Retrospective Studies , Ankle Fractures/surgery , Middle Aged , Adult , Aged , Tobacco Smoking/adverse effects , Postoperative Complications/etiology , Postoperative Complications/epidemiology , Case-Control Studies
10.
Int J Mol Sci ; 25(4)2024 Feb 06.
Article in English | MEDLINE | ID: mdl-38396634

ABSTRACT

Neutrophilic inflammation is a prominent feature of chronic obstructive pulmonary disease (COPD). Developmental endothelial locus-1 (Del-1) has been reported to limit excessive neutrophilic inflammation by inhibiting neutrophil adhesion to the vascular endothelial cells. However, the effects of Del-1 in COPD are not known. We investigated the role of Del-1 in the pathogenesis of COPD. Del-1 protein expression was decreased in the lungs of COPD patients, especially in epithelial cells and alveolar macrophages. In contrast to human lung tissue, Del-1 expression was upregulated in lung tissue from mice treated with cigarette smoke extracts (CSE). Overexpression of Del-1 significantly suppressed IL-8 release and apoptosis in CSE-treated epithelial cells. In contrast, knockdown of Del-1 enhanced IL-8 release and apoptosis. In macrophages, overexpression of Del-1 significantly suppressed inflammatory cytokine release, and knockdown of Del-1 enhanced it. This anti-inflammatory effect was mediated by inhibiting the phosphorylation and acetylation of NF-κB p65. Nuclear factor erythroid 2-related factor 2 (Nrf2) activators, such as quercetin, resveratrol, and sulforaphane, increased Del-1 in both cell types. These results suggest that Del-1, mediated by Nrf2, plays a protective role against the pathogenesis of COPD, at least in part through anti-inflammatory and anti-apoptotic effects.


Subject(s)
Interleukin-8 , Pulmonary Disease, Chronic Obstructive , Animals , Humans , Mice , Anti-Inflammatory Agents/pharmacology , Apoptosis/genetics , Endothelial Cells/metabolism , Inflammation/metabolism , Inflammation/pathology , Interleukin-8/genetics , NF-E2-Related Factor 2/metabolism , NF-kappa B/metabolism , Pulmonary Disease, Chronic Obstructive/genetics , Pulmonary Disease, Chronic Obstructive/metabolism , Tobacco Smoking/adverse effects , Calcium-Binding Proteins/metabolism , Cell Adhesion Molecules/metabolism
11.
Sci China Life Sci ; 67(5): 854-864, 2024 May.
Article in English | MEDLINE | ID: mdl-38265598

ABSTRACT

Tobacco smoking is a prevalent and detrimental habit practiced worldwide, increasing the risk of various diseases, including chronic obstructive pulmonary disease (COPD), cardiovascular disease, liver disease, and cancer. Although previous research has explored the detrimental health effects of tobacco smoking, recent studies suggest that gut microbiota dysbiosis may play a critical role in these outcomes. Numerous tobacco smoke components, such as nicotine, are found in the gastrointestinal tract and interact with gut microbiota, leading to lasting impacts on host health and diseases. This review delves into the ways tobacco smoking and its various constituents influence gut microbiota composition and functionality. We also summarize recent advancements in understanding how tobacco smoking-induced gut microbiota dysbiosis affects host health. Furthermore, this review introduces a novel perspective on how changes in gut microbiota following smoking cessation may contribute to withdrawal syndrome and the degree of health improvements in smokers.


Subject(s)
Dysbiosis , Gastrointestinal Microbiome , Tobacco Smoking , Humans , Tobacco Smoking/adverse effects , Dysbiosis/microbiology , Nicotine/adverse effects , Nicotine/metabolism , Animals , Gastrointestinal Tract/microbiology , Smoking Cessation , Pulmonary Disease, Chronic Obstructive/microbiology , Pulmonary Disease, Chronic Obstructive/etiology
12.
Med. oral patol. oral cir. bucal (Internet) ; 29(1): e18-e26, Ene. 2024. ilus, tab
Article in English | IBECS | ID: ibc-229184

ABSTRACT

Background: The popularity of e-cigarettes has increased rapidly in the last decade, particularly among teens andyoung adults, being advertised as a less harmful alternative to conventional tobacco products. However, in vitroand in vivo studies have evidenced a variable quantity of potentially harmful components and some recognizedcarcinogens which may cause DNA damage in oral cells. Additionally, evidence suggests that e-cigarettes mayplay active roles in the pathogenesis of other malignancies, such as lung and bladder cancers. Therefore, this rapidreview aimed to assess the available clinical evidence about using e-cigarettes as a risk factor for oral potentiallymalignant disorders (OPMD) and oral cancer.Material and Methods: A systematic search for English language articles published was performed in PubMed(MEDLINE), Embase, Scopus, and Web of Science. After the study selection process, the authors included twelveclinical studies about OPMD and oral cancer risk in e-cigarette users.Results: The main findings showed the presence of carcinogenic compounds in saliva and morphologic changes,DNA damage, and molecular pathways related to carcinogenesis in the oral cells of e-cigarette users. However,results were inconsistent compared to tobacco smokers and control groups.Conclusions: the current clinical evidence on this topic is limited and insufficient to support using e-cigarettes asa risk factor for OPMD and oral cancer. Nevertheless, dental care professionals should advise patients responsiblyabout the potentially harmful effects of e-cigarettes on the oral mucosa cells. Future long-term and well-designedclinical studies are needed.(AU)


Subject(s)
Humans , Male , Female , Young Adult , Adult , Oral Hygiene/methods , Electronic Nicotine Delivery Systems , Mouth Neoplasms , Tobacco Smoking/adverse effects , Dentistry , Oral Health , Mouth Diseases , Risk Factors
14.
Int J Cancer ; 154(2): 210-216, 2024 Jan 15.
Article in English | MEDLINE | ID: mdl-37728483

ABSTRACT

Tobacco smoking is the most important risk factor for bladder cancer. Previous studies have identified the N-acetyltransferase (NAT2) gene in association with bladder cancer risk. The NAT2 gene encodes an enzyme that metabolizes aromatic amines, carcinogens commonly found in tobacco smoke. In our study, we evaluated potential interactions of tobacco smoking with NAT2 genotypes and polygenic risk score (PRS) for bladder cancer, using data from the UK Biobank, a large prospective cohort study. We used Cox proportional hazards models to measure the strength of the association. The PRS was derived using genetic risk variants identified by genome-wide association studies for bladder cancer. With an average of 10.1 years of follow-up of 390 678 eligible participants of European descent, 769 incident bladder cancer cases were identified. Current smokers with a PRS in the highest tertile had a higher risk of developing bladder cancer (HR: 6.45, 95% CI: 4.51-9.24) than current smokers with a PRS in the lowest tertile (HR: 2.41, 95% CI: 1.52-3.84; P for additive interaction = <.001). A similar interaction was found for genetically predicted metabolizing NAT2 phenotype and tobacco smoking where current smokers with the slow NAT2 phenotype had an increased risk of developing bladder cancer (HR: 5.70, 95% CI: 2.64-12.30) than current smokers with the fast NAT2 phenotype (HR: 3.61, 95% CI: 1.14-11.37; P for additive interaction = .100). Our study provides support for considering both genetic and lifestyle risk factors in developing prevention measures for bladder cancer.


Subject(s)
Arylamine N-Acetyltransferase , Urinary Bladder Neoplasms , Humans , Arylamine N-Acetyltransferase/genetics , Arylamine N-Acetyltransferase/metabolism , Case-Control Studies , Genome-Wide Association Study , Genotype , Prospective Studies , Risk Factors , Smoking/adverse effects , Smoking/genetics , Tobacco Smoking/adverse effects , Tobacco Smoking/genetics , Urinary Bladder Neoplasms/etiology , Urinary Bladder Neoplasms/genetics
15.
BMC Prim Care ; 24(1): 263, 2023 12 05.
Article in English | MEDLINE | ID: mdl-38053058

ABSTRACT

BACKGROUND: Efforts have been invested towards cessation of tobacco use among youths aged 18-35 years, however, motivators for continued tobacco smoking and reasons for quitting are limited in Ugandan settings. Therefore, this study aimed to explore motivations for continued tobacco smoking and reasons for quitting in Wakiso district Uganda. METHODS: This study used explanatory sequential method. Data from a Population-based survey collected from October 2019 to September 2020 was used to select participants for this qualitative study. Twenty-three in-depths interviews were conducted from July to October 2021 among youths (18-35years old) who reported continued tobacco use and those who quit. Data were analyzed using a team-based thematic content approach with the help of NVivo. RESULTS: Data was collected from a total of twenty three participants, fourteen were tobacco quitters and nine were current tobacco smokers. Recurrent habit, desire to complement the use of other drugs, peer pressure, using smoking as a replacement for alcohol consumption, low tobacco prices, smoking as a tradition were reported as motivators for continued tobacco smoking. However, reported reasons for quitting smoking by youths included; packaging health warnings, school based prevention programs, fear of associated health risks due to tobacco use, embarrassment from family members. CONCLUSION: Targeted, and tailored tobacco prevention counselling through family support programs, intensified health education on the risks of smoking, and implementing stronger health warnings on tobacco packaging can be employed to reduce or stop tobacco use among urban youth.


Subject(s)
Smoking Cessation , Adolescent , Humans , Motivation , Smoking/adverse effects , Smoking/epidemiology , Smoking Cessation/methods , Tobacco Smoking/adverse effects , Tobacco Smoking/epidemiology , Uganda/epidemiology
16.
Sci Rep ; 13(1): 20105, 2023 11 16.
Article in English | MEDLINE | ID: mdl-37973812

ABSTRACT

We analyse parental smoking and cessation (quitting) associations with teenager e-cigarette, alcohol, tobacco smoking and other drug use, and explore parental smoking as a mechanism for social reproduction. We use data from Waves 1-3 of Growing Up in Ireland (Cohort '98). Our analytic sample consisted of n = 6,039 participants reporting in all 3 Waves. Data were collected in Waves 1 and 2 when the children were 9 and 13 years old and in Wave 3 at age 17/18 years. Generalized Estimating Equations (GEE) models were used to analyse teenage substance use at Wave 3. Parental smoking was associated with significantly increased risk of all teenage substance use, adjusted odds ratios were aOR2.13 (ever e-cigarette use); aOR1.92 (ever alcohol use); aOR1.88 (current alcohol use); aOR1.90 (ever use of other drugs); aOR2.10 (ever-smoking); and aOR1.91 (current smoking). Primary caregiver smoking cessation (quitting) was associated with a lower risk for teenager current smoking aOR0.62, ever e-cigarette use aOR 0.65 and other drug use aOR 0.57. Primary caregiver smoking behaviour had greater associations than secondary, and age13 exposure more than age 9. Habitus seems to play a role and wealth was protective for teenage smoking. The findings suggest that prevention interventions should target both caregivers and their children.


Subject(s)
Electronic Nicotine Delivery Systems , Smoking Cessation , Substance-Related Disorders , Child , Humans , Adolescent , Smoking/epidemiology , Tobacco Smoking/adverse effects , Tobacco Smoking/epidemiology , Substance-Related Disorders/epidemiology
17.
Lung Cancer ; 186: 107388, 2023 12.
Article in English | MEDLINE | ID: mdl-37820539

ABSTRACT

BACKGROUND: Smoking at diagnosis is associated with worse survival in lung cancer but the effects of quitting smoking on survival remain unclear. METHODS: In a UK multi-centre study (NCT01192256) we followed all 2751 patients with newly diagnosed non-small cell lung cancer (NSCLC) for up to 2 years or until death as part of the observational trial. Patients were offered smoking cessation advice and treatments according to national guidelines and local services. Smoking status was verified by exhaled carbon monoxide levels. Kaplan-Meier survival analysis and Cox Proportional Hazards Modelling examined the effects of quitting smoking on survival at 2 years. FINDINGS: 646 were current smokers at the time of diagnosis. The unadjusted two-year Kaplan-Meier survivor functions for quitters (0.45, 95 %CI 0.37 to 0.53) and continuers (0.32, 0.28 to 0.36) were significantly different (log-rank test p < 0.01). Median survival times were 659 days for quitters and 348 days for continuers. After adjusting for age, sex, stage, performance status, curative intent surgery, radical radiotherapy and comorbidity, the hazard ratio for quitting at diagnosis (0.75, 95 % CI 0.58 to 0.98) indicated a statistically significant reduction in the risk of death across the two-year study period. INTERPRETATION: Quitting smoking is independently and significantly associated with improved survival regardless of stage in NSCLC. We recommend that smoking cessation advice and treatments should be offered to smokers with lung cancer. TRIAL REGISTRATION: ClinicalTrials.gov, identifier NCT01192256. FUNDING: This work was supported by a 2010 Global Research Award for Nicotine Dependence (GRAND), Pfizer.


Subject(s)
Carcinoma, Non-Small-Cell Lung , Lung Neoplasms , Smoking Cessation , Humans , Carcinoma, Non-Small-Cell Lung/diagnosis , Carcinoma, Non-Small-Cell Lung/therapy , Lung Neoplasms/diagnosis , Smoking/adverse effects , Tobacco Smoking/adverse effects , Tobacco Smoking/epidemiology , Male , Female
18.
Eur Rev Med Pharmacol Sci ; 27(16): 7710-7719, 2023 08.
Article in English | MEDLINE | ID: mdl-37667949

ABSTRACT

OBJECTIVE: Environmental tobacco smoke exposure is a well-recognized risk factor for asthma development and poor asthma control in children. However, the relationship between changes in parental smoking habits over time and the prevalence of childhood asthma remains largely unknown. Our objective was to investigate the trends of parental smoking behaviors in relation to childhood wheeze/asthma rates over a 20-year period. SUBJECTS AND METHODS: A standardized questionnaire on household overall smoking and household indoor tobacco smoking (HITS) habits was distributed to 8-9-years-old school children in the context of five cross-sectional surveys conducted in 1998 (n=3,076), 2003 (n=2,725), 2008 (n=2,688), 2013 (n=2,554) and 2018 (n=2,648). RESULTS: The parental overall smoking and HITS rates have substantially decreased during the study period (p-for-trend<0.001). However, while HITS declined among the fathers of asthmatic and non-asthmatic children as well as among the mothers of non-asthmatic ones (p-for-trend<0.001), it remained unchanged in the case of the mothers of asthmatic participants (p-for-trend 0.283). The mothers of asthmatic children consistently reported more HITS than those of non-asthmatic participants, while prevalence changes of current wheeze/asthma over the surveillance period were in complete agreement with changes in maternal HITS (cross-correlation coefficient 0.918 at zero-year lag) but not with paternal smoking behaviors. CONCLUSIONS: Overall and indoor smoking rates of school children's adult family members declined substantially during the 1998-2018 period in Greece. However, no such trend was noted among mothers of asthmatic children, while temporal changes in maternal indoor smoking rates occurred in parallel with those of childhood asthma prevalence.


Subject(s)
Asthma , Smoking , Adult , Child , Female , Humans , Asthma/epidemiology , Cross-Sectional Studies , Greece/epidemiology , Mothers , Prevalence , Smoking/adverse effects , Smoking/epidemiology , Tobacco Smoking/adverse effects , Tobacco Smoking/epidemiology , Male
19.
Endokrynol Pol ; 74(3): 221-233, 2023.
Article in English | MEDLINE | ID: mdl-37695032

ABSTRACT

Various stimulants (VS) are chemicals that disrupt the endocrine system - endocrine homeostasis of the reproductive system - which also known as endocrine-disrupting chemicals (EDCs). These substances are found in the human body, in both the blood and urine, amniotic fluid, or, among others, the adipose tissue. This article presents the current state of knowledge of the effect of EDCs and additional factors such as smoking, alcohol consumption, and cannabis on the gonads. The article is an overview of the impact of EDCs and their mechanism of action, with particular emphasis on gonads, based on databases such as PubMed, EMBASE and Google Scholar, and Web of Science available until May 2022. The impact of human exposure to bisphenol A (BPA) is not fully understood, but it has been shown that phthalates show a negative correlation in anti-androgenic activity in the case of men and women for the anti-Müllerian hormone (AMH). Smoking cigarettes and passive exposure to tobacco have a huge impact on the effects of endocrine disorders in both women and men, especially during the reproductive time. Also, the use of large amounts of cannabinoids during the reproductive years can lead to similar disorders. It has been documented that excessive alcohol consumption leads to disturbed function of the hypothalamus-pituitary-gonadal axis (HPG). Excess caffeine consumption may adversely affect male reproductive function, although this is not fully proven. Therefore, the following publication presents various stimulants (BPA, phthalates, nicotine, alcohol, cannabis) that disrupt the function of the endocrine system and, in particular, affect the function of the gonads.


Subject(s)
Endocrine Disruptors , Gonads , Endocrine Disruptors/adverse effects , Humans , Animals , Gonads/drug effects , Male , Female , Alcohol Drinking/adverse effects , Tobacco Smoking/adverse effects , Cannabinoids/adverse effects , Ethanol/adverse effects , Nicotine/adverse effects
20.
J Prev Med Public Health ; 56(4): 357-367, 2023 Jul.
Article in English | MEDLINE | ID: mdl-37551074

ABSTRACT

OBJECTIVES: The 2018 Basic Health Research (RISKESDAS), conducted by the Ministry of Health of the Republic of Indonesia showed a high prevalence of dental caries (88.8%) in Indonesia and suggested that smoking tobacco was associated with an increased risk of dental caries. This study analyzed the association between tobacco smoking and dental caries in the Indonesian population. METHODS: This was a cross-sectional analysis of secondary data collected from RISKESDAS 2018. The study population included 35 391 Indonesians aged ≥10 years from all 34 provinces. The decayed, missing, and filled teeth (DMFT) index was used to measure dental caries. Smoking status was assessed qualitatively based on smoking activity, and the level of smoking exposure was assessed based on the Brinkman index. A multivariable logistic regression analysis was employed to examine the relationships of smoking status and smoking exposure levels with the DMFT index. RESULTS: Of the population aged ≥10 years, 36% had a DMFT≥8 (females: 37.5%, males: 33.9%). Almost one-fourth (23.4%) were current smokers, and 4.1% were ex-smokers. Furthermore, 26.4% had a Brinkman index ≥400, indicating heavy smoking. According to the multivariate analysis, current smoking status was associated with the risk of DMFT≥8 in males (adjusted odds ratio [aOR], 1.40; 95% CI, 1.27 to 1.55; p<0.001) and overall (aOR, 1.07; 95% CI, 1.00 to 1.14; p=0.037). In females, ex-smoking was associated with a 41% higher risk of DMFT≥8 (aOR, 1.41; 95% CI, 1.07 to 1.84; p=0.014). Heavy smoking was associated with a higher risk of DMFT≥8 in males (aOR, 1.38; 95% CI, 1.25 to 1.52; p<0.001) and females (aOR, 1.24; 95% CI, 1.03 to 1.50; p=0.022). CONCLUSIONS: Tobacco smoking was associated with dental caries in the Indonesian population.


Subject(s)
Dental Caries , Male , Female , Humans , Indonesia/epidemiology , Cross-Sectional Studies , Dental Caries/epidemiology , Dental Caries/etiology , Tobacco Smoking/adverse effects , Tobacco Smoking/epidemiology , Smoking/adverse effects , Smoking/epidemiology , Prevalence
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