Passive smoking as a cause of heart disease.

A vast number of studies on the unfavorable effects of secondhand smoke (SHS) exist within the international literature, the majority of which evaluate longitudinal epidemiological data. Although limited, the experimental studies that assess the acute and short-term effects of exposure to SHS are also increasing in number. They include cellular, animal, and human studies that indicate a number of pathophysiological mechanisms through which the deleterious effects of SHS may arise. This current review evaluates the existing biological evidence regarding the acute health effects of SHS exposure. Analyses on the inhaled toxicants and the carcinogenicity of SHS are included as well as in-depth discussions on the evidence for acute SHS-induced respiratory, cardiovascular, metabolic, endocrine and immune effects, and SHS-induced influences on oxygen delivery and exercise. The influence of the length of exposure and the duration of the observed effects is also described. Moreover, recent findings regarding the underlying pathophysiological mechanisms related to SHS are depicted so as to generate models that describe the SHS-induced effects on different systems within the human body. Based on the presented biological evidence, it is concluded that brief, acute, transient exposures to SHS may cause significant adverse effects on several systems of the human body and represent a significant and acute health hazard. Future research directions in this area include research on the concentrations of tobacco smoke constituents in the alveolar milieu following SHS exposure, individual susceptibility to SHS, as well as the effects of SHS on neurobehavioral activity, brain cell development, synaptic development, and function.

Biological evidence for the acute health effects of secondhand smoke exposure

BACKGROUND Exposure to environmental tobacco smoke (ETS) has been epidemiologically linked to death from ischemic heart disease in nonsmokers. In this study, we evaluated the influence of 3 days, 3 weeks, and 6 weeks of ETS exposure on myocardial infarct size in a rat ischemia/reperfusion model. METHODS AND RESULTS Sprague-Dawley rats exposed to ETS (four Marlboro cigarettes per 15 minutes, 6 hours per day, 5 days per week) for 3 days (n = 24), 3 weeks (n = 21), or 6 weeks (n = 12) and control rats (n = 24, n = 21, and n = 12, respectively) were subjected to 35 minutes of left coronary artery occlusion and 2 hours of reperfusion. Infarct size and risk area were determined by triphenyltetrazolium chloride and phthalocyanine blue staining, respectively. Air nicotine, carbon monoxide, and total particulates were measured during ETS exposure. Serum lipids, plasma carbon monoxide hemoglobin (COHb), nicotine, and cotinine concentrations were measured in additional groups (6 to 13 rats each) exposed to 3 days, 3 weeks, or 6 weeks of ETS and controls. Average air nicotine, carbon monoxide, and total particulate concentrations were 1103 micrograms/m3, 92 ppm, and 60 mg/m3 for the ETS-exposed rats. Infarct size (infarct mass/risk area x 100%) increased significantly in the ETS groups compared with the control groups in a dose-dependent manner (P = .023), with longer exposure associated with larger infarct size. Infarct size nearly doubled with 6 weeks of ETS exposure (61 +/- 5% versus 34 +/- 3% for control, mean +/- SEM). Plasma COHb, nicotine, and cotinine levels increased significantly in the ETS groups in a dose-dependent manner (all P < .001). CONCLUSIONS Exposure to passive smoking increases myocardial infarct size in a rat model of ischemia and reperfusion. This increase of infarct size exhibited a dose-response relation. These results are consistent with epidemiological studies demonstrating that ETS increases the risk of heart death.

Exposure to environmental tobacco smoke increases myocardial infarct size in rats.

Low-Oxygen Packaging of Fresh Meat with Carbon monoxide: Meat Quality, Microbiology, and Safety

In this review, we have sought to examine the epidemiological, basic science, and public health data regarding the association between second-hand smoke (SHS) exposure and the development of coronary heart disease (CHD). SHS increases the risk of CHD by 25-30% according to multiple cohort, case-control, and meta-analytical studies. Physiologic and basic science research suggest that the mechanisms by which SHS affects the cardiovascular system are multiple and include increased thrombogenesis and low-density lipoprotein oxidation, decreased exercise tolerance, dysfunctional flow-mediated vasodilatation, and activation of inflammatory pathways with concomitant oxidative damage and impaired vascular repair. As a result, chronic exposure promotes atherogenesis and the development of cardiovascular disease, increasing the risk of having an acute coronary syndrome (ACS). With the implementation of statewide and nationwide public smoke-free legislation across the United States and Europe, respectively, over the last 10-15 years, there has been a significant and reciprocal decline in the incidence of emergency admissions for ACS by an average 17% despite persistent attempts on the part of the tobacco industry to diminish the correlation between SHS exposure and CHD. These findings underscore the importance of the effects of smoking legislation on community health.

Second-hand tobacco smoke and cardiovascular disease risk: an epidemiological review.

https://www.internationaljournalofcardiology.com/article/0167-5273(91)90354-R/pdf

Indoor passive smoking: its effect on cardiac performance.

Postinfarction cardiac rupture (PCR) up to the present accounts for approximately 20 percent of autopsy infarcted cases, ranking only behind arrhythmias and cardiac failure in the frequency of AMI complications. We re-examined our observations of a previous anatomo-clinical study of 96 patients who underwent autopsy after death from AMI. Sixteen patients had rupture of the free wall of the left ventricle at the site of infarction. All the patients with rupture showed the following statistically significant characteristics (p less than 0.01) if compared to those without rupture: cardiac hypertrophy (heart weight 390 to 1020 gm; mean: 627.5 +/- 201 gm; left ventricular wall thickness 18 mm to 29 mm; mean: 25.17 +/- 3.6 mm), sudden death (6 cases) without premonitory symptoms or with symptoms of less than an hour's duration or reappearance of chest pain not improved by opiates before late death, that occurred 240 to 660 minutes from chest pain, recorded electrocardiograms showing sinus rhythm with unchanged ST-segment (12 cases), atrioventricular block (2 cases) and junctional rhythm (2 cases). Hypertension pre-existing to the infarction was seen in 6 cases with rupture versus 9 cases without rupture (p less than 0.01). Blood pressure, heart weight and wall thickness of the left ventricle are the most increased parameters in the patients with PCR. Preventive measures against these factors can reduce PCR.

Postinfarction cardiac rupture in the nineties: do we know determinating factors?

To compare the effects of Lidocaine (LID) alone or with Magnesium Sulfate (M) on life-threatening ventricular arrhythmias which followed cardioverted prolonged ventricular fibrillation (VF) during an acute myocardial infarction (AMI), we studied 34 (24.63%) out of 138 patients aged from 52 to 83 years (mean: 66.92 + 8.82) with an anterior AMI, who had cardioverted prolonged VF. Twenty patients (58.8%)--Group A--received LID 2 mg/min at constant-rate infusion through a subclavian catheter following a bolus of LID 100 mg, whereas 14 patients (14.2%)--Group B--received LID at the same dose + M 2.5 mg/min. All the patients had continuous monitoring and LID serum level was measured daily by means of immunofluorescent method (TDX Abbot; range 1.5-5 micrograms/ml). Group A had the following mean serum levels of LID; 250 + 0.9; 1.52; 245 +/- 0.9; 3.20 + 1.1. Group B showed: 2.65 + 1.2; 2.80 + 1.8; 3.10 + 1.2; 3.25 + 1.1. Continuous monitoring displayed the following arrhythmias respectively for Group A and Group B: VT 37 times vs 16(P less than 0.05, significant), transiently cardioverted VF during therapy 17 times vs 6(p less than 0.01, significant), 8 deaths from VF vs 6 - 3 from VF and 3 from asystole - (p = NS). LID + M treatment seemed to be more effective than LID alone to reduce life-threatening arrhythmias following cardioverted prolonged VF of AMI but not the deaths. In addition, M would raise moderately LID serum level and this fact, not yet well known, needs further investigation.

Life-threatening arrhythmias after intravenous lidocaine alone or with magnesium in myocardial infarction complicated by ventricular fibrillation.

P069 Ambulatory blood pressure monitoring in passive smoking and atropine. Response in healthy volunteers

Coronary risk factors (CRF) in acute myocardial infarction (AMI) of elderly with and without hypertension

Handle everyday research tasks with reliable, citation-backed results

Your personal Research Agent to handle research tasks with citation-backed results

Popular Tasks used by Researchers

How can I help with your research?

Meet SciSpace

Get more enhanced response by uploading the PDFs you want me to reference.

No relevant PDFs in your library

SciSpace is the AI research assistant for academics. Run systematic literature reviews on 280M+ papers, and write papers with cited sources. Trusted by 1M+ students, PhDs & researchers.

SciSpace | AI for Research

Analyze PDFs

Code & Manuscripts

Funding & Grants

Literature & Patents

Medical & Clinical Data

Systematic Review

Visualize & Present

Web & Data

Build a Google Scholar-like website for your research.

Build a website

Create charts and images for your research

Create a Chart

Write a paper for submission to a journal

Draft a manuscript

Patent Search

Design eye-catching scientific posters in minutes.

Scientific Poster Generation

Systematic Literature Review

One task is running at the moment. Your messages will be shown right after.

Drag and drop or click here to browse

Loved by <highlight>1 million+</highlight> researchers

Extract a list of specific topics and their sources from unstructured text

Topics

Compare and analyze relevant papers that matches with your search

Papers

Get insights from PDFs and bookmarked papers from your library

My library

Recent searches

Try searching for:

Catch AI-generated content in scholarly and non-scholarly content

{ai} Detector

Ai Writer

Get PDF Summaries, highlighted text explanations 

Chat with PDF

Effortlessly create in-text citations and bibliographies in APA and 2,500 other formats

Citation generator

Get explanations, summaries, and answers on academic papers

Ease up your research workflow with {scispace}'s cohort of exciting AI tools

Elevate your academic writing skills and convey your ideas the way you want

Paraphraser

Explore our range of reading and writing tools

Your file is being prepared and should be ready in a few minutes. If it's a large file, it might take a bit longer. You can close this window, and we'll email you the file when it's done.

You have reached a maximum limit of <strong>{limit}</strong> columns in the table. Remove at least <strong>1</strong> column to add or create another one.

F. Bertanelli

Author Tools

Chat about Author