1. Can You Drink Alcohol With Prednisone
2. Alcohol Vs Nicotine
3. Can You Drink Alcohol With Amoxicillin
4. Can You Drink Alcohol With Nicotine Patches

Important Safety Information and Indication. Decrease the amount of alcohol you drink while taking CHANTIX until you know if CHANTIX affects your ability to tolerate alcohol. The most common side effects of CHANTIX include nausea (30%), sleep problems (trouble sleeping, vivid, unusual, or strange dreams), constipation, gas and/or vomiting. But alcohol-related problems can occur with lesser amounts of alcohol use. It is best not to drink at all while you are pregnant. If it is hard for you to stop drinking, talk with your obstetrician or other health care professional about your drinking habits. Common Myths about Nicotine Patches for Quitting Smoking. The truth is that you will be 50-70% more successful in quitting by using the nicotine patch. Another myth is that you can overdose on nicotine if you smoke while wearing a patch. I still ordered cigarettes thinking the patch would curb the urge so I would drink the same but.

Associated Data

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Abstract

Background

Abnormalities in the electrocardiographic QT interval duration have been associated with an increased risk of ventricular arrhythmias and sudden cardiac death. However, there is substantial uncertainty about the effect of modifiable factors such as coffee intake, cigarette smoking, alcohol consumption, and physical activity on QT interval duration.

Methods

We studied 7795 men and women from the Third National Health and Nutrition Survey (NHANES III, 1988–1994). Baseline QT interval was measured from the standard 12-lead electrocardiogram. Coffee and tea intake, alcohol consumption, leisure-time physical activities over the past month, and lifetime smoking habits were determined using validated questionnaires during the home interview.

Results

In the fully adjusted model, the average differences in QT interval comparing participants drinking ≥6 cups/day to those who did not drink any were −1.2 ms (95% CI −4.4 to 2.0) for coffee, and −2.0 ms (−11.2 to 7.3) for tea, respectively. The average differences in QT interval duration comparing current to never smokers was 1.2 ms (−0.6 to 2.9) while the average difference in QT interval duration comparing participants drinking ≥7 drinks/week to non-drinkers was 1.8 ms (−0.5 to 4.0). The age, race/ethnicity, and RR-interval adjusted differences in average QT interval duration comparing men with binge drinking episodes to non-drinkers or drinkers without binge drinking were 2.8 ms (0.4 to 5.3) and 4.0 ms (1.6 to 6.4), respectively. The corresponding differences in women were 1.1 (−2.9 to 5.2) and 1.7 ms (−2.3 to 5.7). Finally, the average differences in QT interval comparing the highest vs. the lowest categories of total physical activity was −0.8 ms (−3.0 to 1.4).

Conclusion

Binge drinking was associated with longer QT interval in men but not in women. QT interval duration was not associated with other modifiable factors including coffee and tea intake, smoking, and physical activity.

Introduction

Extremely abnormal prolongation or reduction of the electrocardiographic QT interval duration, such as seen in individuals with Mendelian forms of long or short QT syndromes, is associated with increased risk of ventricular arrhythmias and sudden cardiac death –. Furthermore, population studies have also shown associations between smaller increases in QT interval duration and total mortality, cardiovascular mortality, and sudden cardiac death –.

Besides genetic disorders and pharmacologic agents that can cause marked prolongation or shortening of the QT interval , other factors associated with less extreme QT interval variability in the general population include age, sex, hypertension, body mass index, low-calorie diets, electrolytes –, and common genetic variants . However, there is substantial uncertainty about the association of modifiable factors, such as coffee intake, cigarette smoking, alcohol consumption, and physical activity with QT interval duration –. Although several studies have assessed the effect of individual risk factors on QT interval, many of them were small and/or based on selected samples, resulting in inconsistent findings. The purpose of this analysis was thus to investigate the association of coffee, tea, or alcohol intake, smoking, and physical activity with QT interval duration in a large representative sample of the general US population.

The NHANES III study was conducted by the National Center for Health Statistics (NCHS) of the Centers for Disease Control and Prevention (CDC). It is a national survey that collects extensive health information of the general US population from both interviews and medical examinations. The NHANES III study was approved by the NCHS Research Ethics Review Board (ERB), and documented consent was obtained from participants.

Methods

Study Population

We analyzed data from the Third National Health and Nutrition Examination Survey (NHANES III), a cross-sectional study conducted between 1988 and 1994 that used a multistage stratified clustered probability design to select a representative sample of the civilian non-institutionalized US population . The present study was restricted to participants 40 years of age and older as 12-lead electrocardiograms (ECGs) were only performed in this age group. Of the 8,561 participants 40 years of age or older who had available ECG measurements, we excluded 194 participants with missing QT interval duration or heart rate, 535 participants with QRS ≥120 ms, and 37 participants with missing data on coffee, tea, or alcohol intake, smoking, or physical activity. The final analysis was based on 7,795 participants (3,682 men and 4,113 women).

Data collection

NHANES III included a standardized questionnaire administered in the home by a trained interviewer and a detailed physical examination at a mobile examination center. Demographics, education, medical history, and medication use were assessed by interview. QT-prolonging medications were defined according to the Arizona Center for Education and Research on Therapeutics database [36]. Height and weight were measured and body mass index was calculated as weight in kilograms divided by height in meters squared. Blood pressure was measured three times during the in-home interview and three additional times during the participant’s visit to the mobile examination center. Laboratory tests included total cholesterol, HDL cholesterol, plasma glucose, serum potassium, and serum calcium. Diabetes was defined as a fasting plasma glucose ≥126 mg/dL, a nonfasting plasma glucose ≥200 mg/dL, and/or current use of oral hypoglycemic agents or insulin.

Exposure assessment

Coffee and tea consumption over the past month were determined using a food frequency questionnaire during the home interview . The questionnaire asked how often the participants had regular coffee or tea per month, and we categorized the responses into 0, <1, 1–3, 4–5, and ≥6 cups/day. Based on the U.S. Department of Agriculture food composition sources, we estimated that the caffeine of a cup of coffee or tea were 137 and 47 mg, respectively –, and used the frequency of coffee and tea consumption to estimate caffeine intake. In NHANES III, regular colas and sodas were coded together in one variable. Since not all sodas contain caffeine, we did not include colas when calculating total caffeine intake in the main analyses, but performed sensitivity analyses including the contribution of regular colas and sodas to caffeine, assuming that one drink contained 46 mg of caffeine. Caffeine intake was categorized into quartiles in the analysis.

Participants were asked if they had smoked more than 100 cigarettes in their lifetime and if they were current smokers during the home interview. In addition, serum cotinine, a valid and reliable biomarker of exposure to tobacco smoke, was analyzed using high performance liquid chromatography/atmospheric-pressure ionization tandem mass spectrometry . In the present analysis, current smokers were defined as those who self-reported as current smokers, or those who had serum cotinine >10 ng/ml [40]. Former smokers were those participants who had smoked more than 100 cigarettes but were not current smokers. Participants who had not smoked more than 100 cigarettes in their lifetime and had serum cotinine <10 ng/ml were considered never smokers. Current smokers were further categorized into quartiles based on pack-years smoked (a pack-year defined as 20 cigarettes/day for 1 year), and serum cotinine concentrations . In addition, never smokers who were exposed to second-hand smoke (SHS exposed never smokers) were further separated from never smokers who were not exposed to passive smoking (SHS unexposed never smokers). Since the detection limit of continine in NHANES III was 0.05 ng/ml, SHS unexposed never smokers were defined as never smokers with cotinine level <0.05 ng/ml, while SHS exposed nonsmoker were defined as never smokers with cotinine level between 0.05 and 10 ng/ml .

Alcohol consumption was also assessed by the food frequency questionnaire. Participants reported the number of times that they drank beer, wine, and hard liquor in the past month and we categorized total alcohol consumption into 4 groups (0, 1–3, 4–6, ≥7 drinks/week). In addition, the frequency of heavy episodic drinking was assessed during the alcohol and drug component of the examination. Participants were classified as binge drinkers if they had at least five alcoholic drinks in a single day during the past 12 months.

Leisure-time physical activity in the past month was ascertained during the home interview. Physical activities were coded and classified according to the rate of energy expenditure using a standardized scheme . Moderate physical activities included walking, biking, swimming, aerobics, dancing, calisthenics, gardening, lifting weights, and other physical activities if they met age-specific cut-offs of metabolic equivalents (METs): ≥3.0 METs for ages 20–39 years; ≥2.5 METs for ages 40–64 years; ≥2.0 METs for ages 65–79 years; and ≥1.26 METs for age 80 years or older. Vigorous physical activity included jogging or running. In addition, swimming and aerobics were classified as vigorous for participants 40 years or older; biking, dancing, gardening, and calisthenics were classified as vigorous for participants 65 years or older; and walking and lifting weights were classified as vigorous for participants 80 years and older. Other physical activities were also considered vigorous if they met age-specific MET cut-offs: ≥7.2 METs for ages 20–39 years, ≥6.0 METs for ages 40–64 years, ≥4.8 METs for ages 65–79 years, and ≥3.0 METs for age 80 years and older . Total (moderate or vigorous) physical activity was categorized into 0, <3, 3–7.9, and ≥8 times/week. Vigorous physical activity was categorized into 0, <1, 1–4, and >4 times/week.

QT interval

Standard 12-lead resting ECG recordings were performed using a Marquette MAC 12 electrocardiograph (Marquette Medical Systems, Inc., Milwaukee, WI, USA) with signals sampled at 250 samples per second per channel. A representative P-QRS-T cycle was then derived by selective averaging using the Dalhousie ECG Analysis Program . Resting heart rates and QT intervals were obtained from the ECGs. All ECGs were read centrally at the Epidemiological Cardiology Research Center, EPICARE (Wake Forest University, Winston-Salem, NC).

Statistical Analysis

The ECG sampling weights were used in the analysis to account for the complex sampling design . The primary effect measure was the adjusted difference and 95% confidence interval (CI) in QT interval duration by categories of each exposure compared to the reference category, calculated from multivariable linear regression models. We used four models with progressive degrees of adjustment. First, we adjusted for age (continuous), race-ethnicity (non-Hispanic white, non-Hispanic black, Mexican-American, other), sex, and RR-interval (restricted quadratic splines with knots at the 5^th, 50^th, and 95^th percentiles). Second, we further adjusted for BMI (continuous), high school education (yes, no), annual household income (<$20,000, ≥$20,000), and use of QT-prolonging medications (yes, no). Third, we further adjusted for systolic blood pressure, blood pressure lowering medication, total and HDL cholesterol, diabetes, history of myocardial infarction, history of congestive heart failure, serum potassium (continuous), and serum calcium (continuous). Finally, fully adjusted models further included all exposures of interest (i.e., coffee, tea, and alcohol intake, smoking, and physical activity) in a single model. Tests for linear trend across categories of each exposure were computed by including a variable with the median value for each category of exposure in the linear regression models.

Seconday analyses included stratified analysis by sex (as women tend to have longer QT intervals than men), and sensitivity analysis using Bazett’s corrected QT interval as the outcome (Table S1; results were similar to the main analysis). All statistical analyses were conducted using SUDAAN (version 10.0; Research Triangle Institute, Research Triangle Park, NC).

Results

The average age of study participants was 56.5 years, and 45.1% of them were male (Table 1). Non-Hispanic whites comprised 80.7% of the study population. The average duration of the QT interval was 406.3 ms.

Table 1

In the fully adjusted model, the average differences in QT interval comparing participants drinking ≥6 cups/day to those who did not drink any were −1.2 (95% CI −4.4 to 2.0) for coffee, and −2.0 ms (−11.2 to 7.3) for tea, respectively (Table 2). The average difference in QT interval comparing the highest vs. the lowest quartiles of caffeine intake was −1.2 ms (−2.7 to 0.3). With respect to smoking, the average differences in QT interval duration comparing current and former smokers to never smokers in fully adjusted models were 1.2 ms (−0.6 to 2.9) and 0.4 ms (−0.9, 1.7), respectively (Table 3). Among smokers, the average difference in QT interval comparing the highest vs. the lowest quartiles of pack-years was 2.6 ms (−1.0 to 6.2), while the average difference comparing highest vs. the lowest quartiles of serum cotinine concentrations was 1.5 ms (−2.1 to 5.2). SHS exposed never smokers had similar QT interval durations as SHS unexposed never smokers.

Table 2

Table 3

The average difference in QT interval duration comparing participants drinking ≥7 drinks/week to non-drinkers in fully adjusted models was 1.8 ms (−0.5 to 4.0) (Table 4). After adjusting for age, race/ethnicity, sex and RR-interval, the average differences in QT interval duration comparing binge drinking to non-drinkers or to drinkers without binge drinking were 2.2 (0.1 to 4.4) and 3.1 ms (0.8 to 5.3), respectively. In the sex-stratified analysis, the average differences in QT interval comparing binge drinking to non-drinkers or drinkers without binge drinking were 2.8 (0.4 to 5.3) and 4.0 ms (1.6 to 6.4), respectively, among men, and 1.1 ms (−2.9 to 5.2) and 1.7 ms (−2.3 to 5.7), respectively, among women (Table S2). The interaction term for sex and binge drinking was not significant (p-value 0.34), although this analysis was limited by the relatively small number of women with binge drinking (282 women vs. 1005 men).

Table 4

Finally, the average differences in QT interval comparing the highest vs. the lowest categories of total and vigorous physical activity in the fully adjusted model were −0.8 (−3.0 to 1.4) and −0.3 ms (−2.9 to 2.4), respectively (Table 5). When stratified by sex, there was a trend towards shorter QT intervals with increasing levels of total activity in women but not in men in the fully adjusted model (p-trend 0.83 in men and 0.03 in women; p-interaction 0.09, Table S2).

Table 5

Discussion

In a large sample representative of the general US population, we found no association between QT interval duration and coffee or tea intake, cigarette smoking, physical activity, or total alcohol intake, although binge drinking was associated with an increased QT duration particularly in men.

Coffee, tea, and caffeine

Few studies have evaluated the effect of coffee or tea intake on the QT interval, although a few small studies have assessed the short-term effect of caffeine on cardiac repolarization. A study of 18 healthy subjects and 18 patients with frequent ventricular ectopic beats reported no significant change in QT interval in either group after caffeine ingestion (multiple doses of 1 mg/kg of body weight at intervals of one half-life during waking hours) . Another study of 10 healthy volunteers showed that caffeine consumption (400 mg/day, equivalent of 4 cups of coffee) did not affect the QT interval . In addition, experiments with canine ventricular muscle models found no effect of caffeine on cardiac action potentials, which may explain its lack of effect on the QT interval . Our results were consistent with previous research and further suggested that usual intake of caffeine-containing drinks does not affect QT interval duration.

Cigarette smoking

Previous studies have shown conflicting results regarding the influence of acute and chronic smoking on QT interval duration. Some studies have reported longer QT intervals in smokers compared to non-smokers , –, , while others found no significant differences or even shorter QT intervals . Another study showed that smoking cessation reduced the QT interval . Most of these studies had small sample sizes and used only univariate analysis without adjustment for confounders. Furthermore, in some studies the results were dependent on the choice of formula for heart rate correction . Our analysis, with a much larger sample size and more detailed adjustment for potential confounders, suggest a lack of effect of chronic smoking on QT interval duration, although we cannot completely exclude an association between smoking history, reflected in pack-years of smoking, and an increase in QT interval duration.

Alcohol consumption

A substantial body of literature has identified a variety of ECG abnormalities, including prolonged QT interval, in chronic alcoholics or heavy drinkers. Abnormalities of electrolytes (hypomagnesemia, hypopotassemia) –, increased sympathetic tone and catecholamine secretion , as well as cardiac cellular infiltrate, hypertrophy, and fibrosis – are frequently seen in chronic alcoholism, which may all cause changes in QT interval. Electromechanical experiments also suggested a concentration-dependent effect of alcohol on action potential duration, with a decreased duration of repolarization at very high concentrations of alcohol but no effect at low concentrations . Several studies of chronic alcoholics have reported either high incidences of prolonged QT (QTc>440 ms) –, or longer QT intervals compared to normal controls , . In addition, prolongation of the QT interval has also been reported after acute alcohol infusion . In the present analysis, binge drinking, defined as five or more alcoholic drinks in one day during the past 12 months, may identify individuals with excessive heavy alcohol use and who were more likely to have chronic alcoholism. Our results suggested that binge drinking may prolong the QT interval compared to non-drinkers or drinkers without binge drinking, particularly in men. Compared to chronic alcoholism, less is known about the effect of social drinking on QT interval duration in the general population. The only population-based study we could identify (2,894 healthy men and women) showed no association between alcohol intake and QT duration . Our data confirmed this observation that usual alcohol consumption was not associated with QT interval duration.

Physical activity

We did not find an association between physical activity and QT interval duration. When stratified by sex, the results suggested a trend towards shorter QT intervals with increasing levels of total activity in women but not in men. However, the test for interaction between sex and total physical activity was not significant, and a similar trend was not observed for vigorous physical activity. A previous study reported that high physical activity was associated with an increase in QT interval in men but not women . It was hypothesized that a higher left ventricular mass could explain this association , and that this effect may only be observed at very high levels of physical activity. Differences in study population, levels of physical activity, and measurement of physical activity may explain the discrepancy with our findings.

Several limitations of our study need to be considered. First, all exposure factors and QT interval duration were measured at a single time at baseline, which may result in non-differential measurement error as there is substantial within person variability in all these variables. It is thus possible that our analysis may have missed some small associations between exposure factors and QT interval duration. Second, coffee, tea, alcohol, smoking and physical activity are associated with many other behaviors and cardiovascular risk factors, and we cannot exclude residual confounding. Third, the currenly analysis could not differentiate between the acute and long-term effect of each exposure factor due to the limited information available regarding duration and magnitude of exposure. Finally, QT interval duration is an intermediate physiological variable, and the impact of the observed changes on clinical cardiovascular events is uncertain. Some major strengths of this study are its large sample size, the careful standardization and detailed quality control procedures of NHANES, and the generalizability of the findings to the general US population.

In conclusion, data from NHANES III, a large sample representative of the general US population, found no association between QT interval duration and coffee or tea intake, smoking, physical activity and usual drinking, but suggested an association between binge drinking and longer QT interval in men. Future studies are needed to further elucidate the biological mechanisms underlying the observed association between binge drinking and QT interval duration and the role of heavy alcohol intake in QT abnormalities and arrhythmia triggering in the general population.

Supporting Information

Table S1

Adjusted difference (95%CI) in Bazett’s equation-corrected QT (QTb) interval duration.

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Table S2

Adjusted difference (95%CI) in QT interval by sex.

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Footnotes

Competing Interests: The authors have declared that no competing interests exist.

Funding: The present study was funded in part by grants from the National Center for Cardiovascular Research (CNIC Translational Cardiology grant 2008-03), the National Institutes of Health (grants ES015597 and HL091062), the Donald W. Reynolds Cardiovascular Clinical Research Center at Johns Hopkins University and the Fondation Leducq. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. No additional external funding was received for this study.

References

Can You Drink Alcohol With Prednisone

Alcohol Vs Nicotine

Nicotine poisoning describes the symptoms of the toxic effects of nicotine following ingestion, inhalation, or skin contact. Nicotine poisoning can potentially be deadly, though serious or fatal overdoses are rare.^[1] Historically, most cases of nicotine poisoning have been the result of use of nicotine as an insecticide.^[2][3] More recent cases of poisoning typically appear to be in the form of Green Tobacco Sickness, or due to unintended ingestion of tobacco or tobacco products or consumption of nicotine-containing plants.^[4][5][6]

The estimated lower limit of a lethal dose of nicotine has been reported as between 500 and 1000 mg.^[7] Children may become ill following ingestion of one cigarette;^[8] ingestion of more than this may cause a child to become severely ill.^[5][9] The nicotine in the e-liquid of an electronic cigarette can be hazardous to infants and children, through accidental ingestion or skin contact.^[10] In some cases children have become poisoned by topical medicinal creams which contain nicotine.^[11]

People who harvest or cultivate tobacco may experience Green Tobacco Sickness (GTS), a type of nicotine poisoning caused by skin contact with wet tobacco leaves. This occurs most commonly in young, inexperienced tobacco harvesters who do not consume tobacco.^[4][12]

Signs and symptoms[edit]

Nicotine poisoning tends to produce symptoms that follow a biphasic pattern. The initial symptoms are mainly due to stimulatory effects and include nausea and vomiting, excessive salivation, abdominal pain, pallor, sweating, hypertension, tachycardia, ataxia, tremor, headache, dizziness, muscle fasciculations, and seizures.^[4] After the initial stimulatory phase, a later period of depressor effects can occur and may include symptoms of hypotension and bradycardia, central nervous system depression, coma, muscular weakness and/or paralysis, with difficulty breathing or respiratory failure.^[1][4][14]

From September 1, 2010 to December 31, 2014, there were at least 21,106 traditional cigarette calls to US poison control centers.^[15] During the same period, the ten most frequent adverse effects to traditional cigarettes reported to US poison control centers were vomiting (80.0%), nausea (9.2%), drowsiness (7.8%), cough (7.2%), agitation (6.6%), pallor (3.0%), tachycardia (2.5%), diaphoresis (1.5%), dizziness (1.5%), and diarrhea (1.4%).^[15] 95% of traditional cigarette calls were related to children 5 years old or less.^[15] Most of the traditional cigarette calls were a minor effect.^[15]

Calls to US poison control centers related to e-cigarette exposures involved inhalations, eye exposures, skin exposures, and ingestion, in both adults and young children.^[16] Minor, moderate, and serious adverse effects involved adults and young children.^[15] Minor effects correlated with e-cigarette liquid poisoning were tachycardia, tremor, chest pain and hypertension.^[17] More serious effects were bradycardia, hypotension, nausea, respiratory paralysis, atrial fibrillation and dyspnea.^[17] The exact correlation is not fully known between these effects and e-cigarettes.^[17] 58% of e-cigarette calls to US poison control centers were related to children 5 years old or less.^[15] E-cigarette calls had a greater chance to report an adverse effect and a greater chance to report a moderate or major adverse effect than traditional cigarette calls.^[15] Most of the e-cigarette calls were a minor effect.^[15]

From September 1, 2010 to December 31, 2014, there were at least 5,970 e-cigarette calls to US poison control centers.^[15] During the same period, the ten most frequent adverse effects to e-cigarettes and e-liquid reported to US poison control centers were vomiting (40.4%), eye irritation or pain (20.3%), nausea (16.8%), red eye or conjunctivitis (10.5%), dizziness (7.5%), tachycardia (7.1%), drowsiness (7.1%), agitation (6.3%), headache (4.8%), and cough (4.5%).^[15]

Toxicology[edit]

The LD₅₀ of nicotine is 50 mg/kg for rats and 3 mg/kg for mice. 0.5–1.0 mg/kg can be a lethal dosage for adult humans, and 0.1 mg/kg for children.^[18][19] However the widely used human LD₅₀ estimate of 0.5–1.0 mg/kg was questioned in a 2013 review, in light of several documented cases of humans surviving much higher doses; the 2013 review suggests that the lower limit causing fatal outcomes is 500–1000 mg of ingested nicotine, corresponding to 6.5–13 mg/kg orally.^[20] An accidental ingestion of only 6 mg may be lethal to children.^[21]

It is unlikely that a person would overdose on nicotine through smoking alone. The US Food and Drug Administration (FDA) stated in 2013: 'There are no significant safety concerns associated with using more than one [over the counter] OTC [nicotine replacement therapy] NRT at the same time, or using an OTC NRT at the same time as another nicotine-containing product—including a cigarette.'^[22][23][24] Ingestion of nicotine pharmaceuticals, tobacco products, or nicotine containing plants may also lead to poisoning.^[4][5][6] Smoking excessive amounts of tobacco has also led to poisoning; a case was reported where two brothers smoked 17 and 18 pipes of tobacco in succession and were both fatally poisoned.^[2] Spilling an extremely high concentration of nicotine onto the skin can result in intoxication or even death since nicotine readily passes into the bloodstream following skin contact.^[25][26]

The recent rise in the use of electronic cigarettes, many forms of which are designed to be refilled with nicotine-containing 'e-liquid' supplied in small plastic bottles, has renewed interest in nicotine overdoses, especially in the possibility of young children ingesting the liquids.^[27] A 2015 Public Health England report noted an 'unconfirmed newspaper report of a fatal poisoning of a two-year old child' and two published case reports of children of similar age who had recovered after ingesting e-liquid and vomiting.^[27] They also noted case reports of suicides by nicotine, where adults drank liquid containing up to 1,500 mg of nicotine.^[27] They recovered (helped by vomiting), but an ingestion apparently of about 10,000 mg was fatal, as was an injection.^[27] They commented that 'Serious nicotine poisoning seems normally prevented by the fact that relatively low doses of nicotine cause nausea and vomiting, which stops users from further intake.'^[27] Four adults died in the US and Europe, after intentionally ingesting liquid.^[28] Two children, one in the US in 2014 and another in Israel in 2013, died after ingesting liquid nicotine.^[29]

The discrepancy between the historically stated 60-mg dose and published cases of nicotine intoxication has been noted previously (Matsushima et al. 1995; Metzler et al. 2005). Nonetheless, this value is still widely accepted over the 500mg figure as the basis for safety regulations of tobacco and other nicotine-containing products (such as the EU wide TPD, set at a maximum of 20mg.

Pathophysiology[edit]

The symptoms of nicotine poisoning are caused by effects at nicotinic cholinergic receptors. Nicotine is an agonist at nicotinic acetylcholine receptor which are present in the central and autonomic nervous systems, and the neuromuscular junction. At low doses nicotine causes stimulatory effects on these receptors, however, higher doses or more sustained exposures can cause inhibitory effects leading to neuromuscular blockade.^[4][30]

It is sometimes reported that people poisoned by organophosphate insecticides experience the same symptoms as nicotine poisoning. Organophosphates inhibit an enzyme called acetylcholinesterase, causing a buildup of acetylcholine, excessive stimulation of all types of cholinergic neurons, and a wide range of symptoms. Nicotine is specific for nicotinic cholinergic receptors only and has some, but not all of the symptoms of organophosphate poisoning.

Diagnosis[edit]

Increased nicotine or cotinine (the nicotine metabolite) is detected in urine or blood, or serum nicotine concentrations increase.

Can You Drink Alcohol With Amoxicillin

Treatment[edit]

The initial treatment of nicotine poisoning may include the administration of activated charcoal to try to reduce gastrointestinal absorption. Treatment is mainly supportive and further care can include control of seizures with the administration of a benzodiazepine, intravenous fluids for hypotension, and administration of atropine for bradycardia. Respiratory failure may necessitate respiratory support with rapid sequence induction and mechanical ventilation. Hemodialysis, hemoperfusion or other extracorporeal techniques do not remove nicotine from the blood and are therefore not useful in enhancing elimination.^[4] Acidifying the urine could theoretically enhance nicotine excretion,^[31] although this is not recommended as it may cause complications of metabolic acidosis.^[4]

Prognosis[edit]

The prognosis is typically good when medical care is provided and patients adequately treated are unlikely to have any long-term sequelae. However, severely affected patients with prolonged seizures or respiratory failure may have ongoing impairments secondary to the hypoxia.^[4][32] It has been stated that if a patient survives nicotine poisoning during the first 4 hours, they usually recover completely.^[14] At least at 'normal' levels, as nicotine in the human body is broken down, it has an approximate biological half-life of 1–2 hours. Cotinine is an active metabolite of nicotine that remains in the blood for 18–20 hours, making it easier to analyze due to its longer half-life.^[33]

References[edit]

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2. ^ ^abMcNally WD (1920). 'A report of five cases of poisoning by nicotine'. Journal of Laboratory and Clinical Medicine. 5: 213–217.
3. ^McNally WD (1923). 'A report of seven cases of nicotine poisoning'. Journal of Laboratory and Clinical Medicine. 8: 83–85.
4. ^ ^abcdefghiSchep, Leo J.; Slaughter, Robin J.; Beasley, D. Michael G. (September–October 2009). 'Nicotinic plant poisoning'. Clinical Toxicology. 47 (8): 771–781. doi:10.1080/15563650903252186. PMID19778187.
5. ^ ^abcSmolinske SC, Spoerke DG, Spiller SK, Wruk KM, Kulig K, Rumack BH (January 1988). 'Cigarette and nicotine chewing gum toxicity in children'. Human Toxicology. 7 (1): 27–31. doi:10.1177/096032718800700105. PMID3346035.
6. ^ ^abFurer V, Hersch M, Silvetzki N, Breuer GS, Zevin S (March 2011). 'Nicotiana glauca (tree tobacco) intoxication—two cases in one family'. Journal of Medical Toxicology. 7 (1): 47–51. doi:10.1007/s13181-010-0102-x. PMC3614112. PMID20652661.
7. ^Mayer B (2014). 'How much nicotine kills a human? Tracing back the generally accepted lethal dose to dubious self-experiments in the nineteenth century'. Arch. Toxicol. 88 (1): 5–7. doi:10.1007/s00204-013-1127-0. PMC3880486. PMID24091634.
8. ^Smolinske SC, Spiller SK, Spoerke DG, Wruk KM, Kulig K, Rumack BH (1985). 'Paediatric nicotine overdose'. Veterinary and Human Toxicology. 28 (4): 308–9.
9. ^Malizia E, Andreucci G, Alfani F, Smeriglio M, Nicholai P (April 1983). 'Acute intoxication with nicotine alkaloids and cannabinoids in children from ingestion of cigarettes'. Human Toxicology. 2 (2): 315–6. doi:10.1177/096032718300200222. PMID6862475.
10. ^Brown, C. J.; Cheng, J. M. (2014). 'Electronic cigarettes: product characterisation and design considerations'. Tobacco Control. 23 (Supplement 2): ii4–ii10. doi:10.1136/tobaccocontrol-2013-051476. ISSN0964-4563. PMC3995271. PMID24732162.
11. ^Davies P, Levy S, Pahari A, Martinez D (December 2001). 'Acute nicotine poisoning associated with a traditional remedy for eczema'. Archives of Disease in Childhood. 85 (6): 500–2. doi:10.1136/adc.85.6.500. PMC1718993. PMID11719343.
12. ^Gehlbach SH, Williams WA, Perry LD, Woodall JS (September 1974). 'Green-tobacco sickness. An illness of tobacco harvesters'. JAMA. 229 (14): 1880–3. doi:10.1001/jama.1974.03230520022024. PMID4479133.
13. ^Detailed reference list is located at a separate image page.
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External links[edit]

Can You Drink Alcohol With Nicotine Patches