Tobacco use and urinary excretion of thromboxane A2 and prostacyclin metabolites in women stratified by age.

Rångemark, Christina; Benthin, Günther; Granström, Elisabeth; Persson, Lennart; Winell, S.; Wennmalm, Åke

doi:10.1161/01.cir.86.5.1495

Cited by 41 publications

(30 citation statements)

References 27 publications

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“…75 ) Smith and colleagues 85 concluded that SHS exposure levels did not activate platelets in "typical home environments" because no difference in urinary thromboxane and prostacyclin was observed between nonsmokers from nonsmoking homes and nonsmokers from smoking homes. However, Smith's smoker "control group" did not demonstrate significantly elevated thromboxane relative to the 2 nonsmoker groups, which contradicted previous tobacco industry-funded literature 94,95 demonstrating that active smoking was associated with thromboxane release. In the discussion, Smith and his coauthors acknowledged this inconsistency but argued that the active smokers in the study reacted differently because of large smoke exposures.…”

Section: Attacking Biological Plausibility: Rjr Experimentscontrasting

confidence: 63%

“…104 Reviewers 125 of the manuscript for Toxicological Sciences questioned the variation in the thromboxane levels because the nonsmokers not exposed to SHS had a higher level of urinary thromboxane than the nonsmokers exposed to SHS. In the final published article, 91 Smith acknowledged that these results were not consistent with previous literature 94,95 suggesting that thromboxane was released with active smoking but suggested that the higher levels were due to an unknown stress (although Smith did not find that oxidative or hormonal stress was significantly associated). Reviewers 125 also noted a failure to comment on other relevant literature such as the 1996 human exposure experiment 106 that demonstrated that repeated daily exposures to SHS over 1 week elevated nonsmoker levels of serum thromboxane to those comparable to active smokers; this literature was not addressed in Smith's final publication.…”

Section: Testing the Hormonal And Oxidative Stress Hypothesismentioning

confidence: 69%

“…93 In previous industry-funded studies, urinary thromboxane and prostacyclin were measured in current smokers, which demonstrated high levels of variability. 94,95 (Urinary thromboxane and prostacyclin are also only indirect measures of functional capacity of platelets, whereas aggregation is the gold standard because platelet behavior is observed directly. 96,97 Urinary measurements of prostacyclin are complex because prostacyclin is produced in a variety of organs, including the kidney.…”

Section: Attacking Biological Plausibility: Rjr Experimentsmentioning

confidence: 99%

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Tobacco Industry Efforts Undermining Evidence Linking Secondhand Smoke With Cardiovascular Disease

Tong

Glantz

2007

Circulation

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Background-The scientific consensus that secondhand smoke (SHS) increases cardiovascular disease (CVD) risk by 30% is based on epidemiological and biological evidence. The tobacco industry has contested this evidence that SHS causes CVD, but how and why they have done it has not been described. Methods and Results-About 50 million pages of tobacco industry documents were searched using general keywords and names of industry consultants and scientists. Tobacco industry-funded epidemiological analyses of large data sets were used to argue against an epidemiological association between SHS and CVD and smoke-free regulations, but these analyses all suffered from exposure misclassification problems that biased the results toward the null. More recent industry-funded publications report an increased risk of CVD associated with SHS but claim a low magnitude of risk. When early tobacco industry-funded work demonstrated that SHS increased atherosclerosis, the industry criticized the findings and withdrew funding. RJ Reynolds focused on attacking the biological plausibility of the association between SHS and CVD by conducting indirect platelet aggregation studies, exposure chamber experiments, and literature reviews. Although these studies also suffered from exposure misclassification problems, several produced results that were consistent with a direct effect of SHS on blood and vascular function. Instead, RJ Reynolds attributed these results to an unproven epinephrine-related stress response from odor or large smoke exposure, which supported their regulatory and "reduced-harm" product development efforts. Philip Morris' recent "reduced-harm" efforts seem supportive of a similar corporate agenda. Conclusions-The tobacco industry attempted to undermine the evidence that SHS causes CVD to fight smoke-free regulations while developing approaches to support new products that claim to reduce harm. The industry interest in preserving corporate viability has affected the design and interpretation of their cardiovascular studies, indicating the need for great caution in current debates about future tobacco industry regulation and development of reduced-harm tobacco products.

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Section: Attacking Biological Plausibility: Rjr Experimentscontrasting

confidence: 63%

Section: Testing the Hormonal And Oxidative Stress Hypothesismentioning

confidence: 69%

Section: Attacking Biological Plausibility: Rjr Experimentsmentioning

confidence: 99%

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Tobacco Industry Efforts Undermining Evidence Linking Secondhand Smoke With Cardiovascular Disease

Tong

Glantz

2007

Circulation

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“…15 Similar signs of a reversible effect of smoking on Tx-M excretion were recently obtained in a study on smoking and nonsmoking women aged 18-59 years. 27 Controlled studies on the change in Tx-M excretion immediately after cessation of smoking have, however, not been reported.…”

Section: Discussionmentioning

confidence: 99%

“…27 In that study former smokers did not differ from lifelong nonsmokers in excretion of Tx-M. To further characterize the apparent reversibility in the effect of smoking, we followed urinary excretion of the TxA 2 metabolites Tx-M and ll-dehydro-TxBj (dTx) 2829 in women who were quitting habitual smoking. We also determined the urinary excretion of 2,3-dinor-6-keto-prostaglandin F lo (PGI-M), a metabolite of prostacyclin, 30 ' 31 since it has been proposed that an increased formation of prostacyclin in the vascular endothelium may reflect an increased interaction between the platelets and the vascular endothelium.…”

mentioning

confidence: 94%

Excretion of thromboxane metabolites in healthy women after cessation of smoking.

Rångemark

Ciabattoni

Wennmalm

1993

Arterioscler Thromb

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Cigarette smokers, but not former smokers, excrete more thromboxane A 2 (TxA 2 ) metabolites in the urine than do lifelong nonsmokers, which suggests chronic activation of their platelets. To further characterize the effect elicited by smoking on platelet function, we followed the change in urinary excretion of the 2,3-dinor (Tx-M) and 11-dehydro (dTx) metabolites of TxAj, analyzed by gas chromatography/mass spectrometry and radioimmunoassay, respectively, in eight healthy women who quit habitual smoking and compared it with the recovery of these metabolites after a single dose of acetylsalicylic acid (ASA). Tx-M and dTx before cessation of smoking were approximately 550 and 600 pg/mg creatinine, respectively. Within 3 days after quitting smoking, Tx-M and dTx had dropped to stable levels of approximately 300 and 350 pg/mg, respectively. The rates of change in excretion of Tx-M and dTx after smoking cessation were more rapid (p<0.02 and 0.02, respectively) than those observed during the recovery of platelet function after a single dose of ASA. The excretion of 2,3-dinor-6-keto-prostaglandin ¥ l a , a metabolite of prostacyclin, was not affected by smoking cessation. We conclude that cigarette smoking elicits an increase in platelet activity in the absence of vascular injury. This increase is reversible within the life span of the platelets. {Arteriosclerosis and Thrombosis 1993;13:777-782) KEY WORDS • acetylsalicylic acid • cardiovascular risk factors • cigarette smoking • platelets • prostacyclin • thromboxanes • urineC igarette smoking is a major risk factor for cardiovascular disease; the risk increases progressively as daily cigarette consumption increases.1 " 5 After cessation of smoking the risk drops rather rapidly toward the level observed in nonsmokers. 6 -9 Platelets are thought to play an important role in cardiovascular disease, 10 ' 11 but the effect of smoking on platelet function is poorly understood. Smokers have been reported to display biochemical evidence of increased activation of platelets in vivo. "15 These data may indicate facilitation of platelet aggregability as a significant etiologic factor in smoking-associated cardiovascular disease.Thromboxane A 2 (TxA 2 ) is formed in platelets from arachidonic acid.16 TxA 2 has platelet proaggregatory and proadhesive properties and is also a strong vasoconstrictor. The administration of acetylsalicylic acid (ASA) in doses that inhibit cyclooxygenase-dependent formation of TxA 2 in platelets has proven efficient in the primary 17 and secondary 18 prevention of acute myocardial infarction. These data indicate that TxA 2 formed in platelets is etiologically involved in certain acute cardio- Received November 18, 1992; revision accepted February 12, 1993. vascular disorders as well as being a marker for platelet activity.Cigarette smoking is linked to an increased incidence of cardiovascular disease in women.19 " 22 Although women seem to develop cardiovascular disease 10-15 years later than men, 23 it is a leading cause of death among women. ...

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Transdermal Nicotine Replacement Therapy in Cigarette Smokers with Acute Subarachnoid Hemorrhage

et al. 2010

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Despite vasoactive properties, administration of NRT among active smokers with acute SAH appeared to be safe, with similar rates of vasospasm and DCI, and a slightly higher rate of seizures. The association of NRT with lower mortality could be due to chance, to uncontrolled factors, or to a neuroprotective effect of nicotine in active smokers hospitalized with SAH, and should be tested prospectively.

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Tobacco use and urinary excretion of thromboxane A2 and prostacyclin metabolites in women stratified by age.

Cited by 41 publications

References 27 publications

Tobacco Industry Efforts Undermining Evidence Linking Secondhand Smoke With Cardiovascular Disease

Tobacco Industry Efforts Undermining Evidence Linking Secondhand Smoke With Cardiovascular Disease

Excretion of thromboxane metabolites in healthy women after cessation of smoking.

Transdermal Nicotine Replacement Therapy in Cigarette Smokers with Acute Subarachnoid Hemorrhage

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