Secondhand Smoke Exposure and Cardiovascular Effects Making Sense of the Evidence (2010) / Chapter Skim
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3 Experimental Studies Relevant to the Pathophysiology of Secondhand Smoke
3 Experimental Studies Relevant to the Pathophysiology of Secondhand Smoke
Pages 59-94
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From page 59... ...
Cigarette smoke, either mainstream or secondhand smoke, could produce cardiovascular disease by a number of interrelated modes of action, including oxidative stress, hemodyamic and autonomic effects, endothelial
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From page 60... ...
Although those physiological changes have been observed and used to assess possible modes of action of secondhand smoke, to date most have not been formally validated as clinical tests and there is not a consensus within the scientific community that they are predictive of actual clinical disease (Ledford, 2008; Wang, 2008; WHO, 2007)
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From page 61... ...
The exact mechanisms whereby oxidative stress leads to cardiovascular disease, such as atherosclerosis, are not clear, but it appears that oxidative stress may play a role in cardiovascular pathophysiology (Ballinger et al., 2002) , and it could account for many effects of tobacco-smoke exposure, such as endothelial dysfunction, thrombosis, and inflammation (Raupach et al., 2006; Thomas et al., 2008)
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From page 62... ...
The role of oxidative stress was assessed by looking at the interactions between glutathione S-transferase (GST) deficiency, which exhibits antioxidative properties, and the effects of secondhand smoke exposure on heart rate variability (HRV)
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From page 63... ...
Nicotine acts on nicotinic cholinergic receptors in the brain and adrenal glands to activate the sympathetic nervous system, and this leads to epinephrine release. Nicotine thus acts as a sympathomimetic drug in increasing heart rate, blood pressure, and cardiac contractility and constricting some blood vessels (Haass and Kubler, 1997)
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From page 64... ...
(2008) further examined the vascular effects of secondhand smoke exposure to assess whether the effects are mediated by a nonspecific reaction to smoke, or are more unique to tobacco smoke, the role of nicotine in the effects, the persistence of the effects following cessation of exposure, and the effect of secondhand smoke on microvascular function measured by skin blood flow.
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From page 65... ...
The secondhand-smoke exposure increased endothelial progenitor cells (EPCs) and plasma vascular endothelial growth factor but eliminated EPC chemotaxis and decreased endothelial function as measured by flow-mediated dilation (FMD)
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From page 66... ...
Following exposure to secondhand smoke brachial and aortic systolic blood pressure increased in males but not females, and an abnormality was observed in the radial and aortic pressure waveforms; no changes were seen in brachial or aortic diastolic blood pressure, heart rate, or left ventricular ejection duration in either sex. No changes were seen in a control group (6 men, 6 women)
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From page 67... ...
; platelets also can adhere to damaged vascular endothelium. Adherence of platelets increases thrombus formation, disrupts the coronary artery lining, speeds progression of atherosclerotic lesions, and is associated with increased risk of ischemic heart disease (Law and Wald, 2003)
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From page 68... ...
examined the relationship between secondhandsmoke exposure, measured as plasma cotinine, and biomarkers of heartdisease risk -- including CRP, homocysteine, fibrinogen, and white-cell count -- in 7,599 never-smokers in the third National Health and Nutrition Examination Survey (NHANES III)
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From page 69... ...
Gonadal hormones, however, were decreased following secondhand smoke exposure in both men and women. Hyperlipidemia Cigarette-smoking is associated with low high-density lipoprotein cholesterol (HDL-C)
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(2006) compared secondhand-smoke exposure, ascertained by a questionnaire administered by an interviewer and serum cotinine concentrations, and time to develop glucose intolerance in the Coronary Artery Risk Development in Young Adults (CARDIA)
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From page 71... ...
These data are from experimental studies in cells or animals or, in some cases, intentional human-dosing studies. Some of the effects in cell systems or animals are seen with exposures above those seen in humans following secondhand-smoke exposure.
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From page 72... ...
SECONDHAND SMOKE EXPOSURE TABLE 3-1 Known Cardiovascular Toxicity of Cigarette Smoke Constituentsa Cardiovascular Risk Categoryb Compound Toxicity Carbon monoxide Moderate Suppression of cardiac function, S-T depression in patients with stable CAD Nicotine High Hemodynamic changes Acetaldehyde Low Acetic acid Low Nitrogen oxides Low Formaldehyde Medium Hypertension, atherosclerosis Benzene Moderate Tachycardia, arrhythmia, arterial hypertension Acetone Low Catechol Low 1,3-butadiene Moderate Atherosclerosis Toluene Low Methanol Low Hydroquinone Low Phenol Low Acrolein High Hypertension; atherogenesis, decreased plaque stability, increased thrombosis; suppression of coronary flow and cardiac contractility Methylethylketone Low Propionaldehyde Low Pyridine Moderate Carbon disulfide Moderate Hypertension, ischemic heart disease, thrombosis, hypercholesterolemia, arrhythmias, decreased cardiac output 3-vinylpyridine Moderate Atherosclerosis Cholesterol Low Crotonaldehyde High Hypertension, atherogenesis, decrease in plaque stability, increased thrombosis; suppression of coronary flow and cardiac contractility Butyraldehyde Moderate Hypertension
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From page 73... ...
Epidemiologic data indicate that occupational exposure to aldehydes increases the risk of cardiovascular disease. The increased risk of atherosclerotic heart disease in workers in plants that produce formaldehyde (Stewart et al., 1990)
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From page 74... ...
, and chronic exposure to 1,3-butadiene has also been linked to an increase in risk of cardiovascular disease. In a case–control cohort study of workers in a styrene-butadiene manufacturing plant in the United States from 1943 to 1982, black workers had a significantly increased standardized mortality ratio (SMR)
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From page 75... ...
although the incidence of plaque development was not significantly different between the exposed and unexposed groups. Acute effects of butadiene on endothelial function or hemodynamics have not been reported, and the cardiovascular disease risk posed by butadiene at concentrations present in secondhand smoke has not been assessed directly.
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From page 76... ...
Nevertheless, the effects of low-dose human or animal exposure to CS2 in tobacco smoke on cardiovascular disease have not been examined. Benzene Tobacco smoke contains relatively high concentrations of benzene.
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From page 77... ...
Nonetheless, because we cannot definitively exclude any contribution of nicotine, we briefly review here some of the concerns about nicotine and cardiovascular toxicity. Studies of users of smokeless tobacco suggest that nicotine is not a major contributor to cardiovascular disease (Arabi, 2006)
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From page 78... ...
The contributions of small doses of nicotine seen in secondhand-smoke exposure to human cardiovascular disease, however, are difficult to predict. Polycyclic Aromatic Hydrocarbons Several PAHs present in tobacco smoke -- including heterocyclines, heterocyclic aromatic amines, and nitro compounds -- have been shown
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From page 79... ...
of fatal ischemic heart disease (1.64) was observed in connection with average benzo[a]
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From page 80... ...
demonstrated that patients exposed to secondhand smoke from 15 cigarettes in 2 hours had elevated venous carboxyhemoglobin, as well as increased resting heart rate, systolic and diastolic blood pressure,
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From page 81... ...
however demonstrated that patients exposed to secondhand smoke from 15 cigarettes in 2 hours had elevated venous carboxyhemoglobin, as well as increased resting heart rate and systolic and diastolic blood pressure, and decreased heart rate and systolic blood pressure at angina. In addition, children exposed to secondhand smoke have been reported to have increased concentrations of 2,3-diphosphoglycerate (Moskowitz et al., 1990)
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From page 82... ...
Increase in demand for oxygen may be a consequence of sympathetic nervous stimulation seen in response to secondhand-smoke exposure (Hausberg et al., 1997) , which could result in an increase in blood pressure and heart rate, as reported in some studies of PM exposure (Brook, 2005; Brook et al., 2003; Delfino et al., 2005)
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From page 83... ...
1989. Acute effects of carbon monoxide exposure on individuals with coronary artery disease.
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From page 84... ...
2003. Cigarette smoking and cardiovascular disease: Pathophysiology and implications for treatment.
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2005. Polycyclic aromatic hydrocarbons and fatal ischemic heart disease.
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2007. Effects of passive smoking on heart rate variability, heart rate and blood pressure: An observational study.
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From page 87... ...
2008. Brief secondhand smoke exposure depresses endothelial progenitor cells activity and endothelial function: Sustained vascular injury and blunted nitric oxide production.
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2002. Cigarette smoke exposure and hyper cholesterolemia increase mitochondrial damage in cardiovascular tissues.
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From page 89... ...
2003. Environmental tobacco smoke and ischemic heart disease.
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From page 90... ...
2004. Acute exposure to environmental tobacco smoke reduces HDL-C and HDL2-C.
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From page 91... ...
2008. Glutathione S-transferase polymorphisms, passive smoking, obesity, and heart rate variability in nonsmokers.
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From page 92... ...
2007. Anti- and pro-oxidant factors and endothelial dysfunction in chronic cigarette smokers with coronary heart disease.
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From page 93... ...
2005. Tobacco smoke exposure is associated with the metabolic syndrome in adolescents.
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