Ethanol Risk Summary

Risk Factor: D*
Class: Central nervous system drugs / Sedatives and hypnotics

Fetal Risk Summary

The teratogenic effects of ethanol (alcohol) have been recognized since antiquity, but this knowledge gradually fell into disfavor and was actually dismissed as superstition in the 1940s (1). Approximately three decades later, the characteristic pattern of anomalies that came to be known as the fetal alcohol syndrome (FAS) were rediscovered, first in France and then in the United States (2,3,4 and 5). By 1981, over 800 clinical and research papers on the FAS had been published (6).

Mild FAS (low birth weight) has been induced by the daily consumption of as little as two drinks (1 ounce of absolute alcohol or about 30 mL) in early pregnancy, but the complete syndrome is usually seen when maternal consumption is four to five drinks (6075 mL of absolute alcohol) per day or more. The Council on Scientific Affairs of the American Medical Association and the American Council on Science and Health have each published reports on the consequences of maternal alcohol ingestion during pregnancy (7,8). The incidence of the FAS, depending upon the population studied, is estimated to be between 1/300 and 1/2000 live births with 30%40% of the offspring of alcoholic mothers expected to show the complete syndrome (7). The true incidence may be even higher because the diagnosis of FAS can be delayed for many years (9) (e.g., see Reference 25 below). In addition, the incidence of alcohol abuse seems to be rising. A 1989 report found that alcohol abuse during 1987 in 1,032 pregnant women was 1.4% compared to 0.7% of 5,602 pregnant women during 19771980 (10). The difference in frequency was significant (p<0.05).

Heavy alcohol intake by the father prior to conception has been suspected of producing the FAS (11,12), although this association has been challenged (13). The report by the AMA Council states that growth retardation and some adverse aspects of fetal development may be due to paternal influence but conclusive evidence for the complete FAS is lacking (7).

Evidence supporting an association between regular drinking by the father in the month before conception and the infant's birth weight was published in two reports, both by the same authors (14,15). Regular drinking was defined as an average of at least 30 ml of ethanol daily or of 75 mL or more on a single occasion at least once a month (14). Occasional drinking was defined as anything less than this. The mean birth weight, 3465 g, of 174 infants of regular drinking fathers was 181 g less than the mean birth weight, 3646 g, of 203 infants of occasional drinking fathers, a significant difference (p<0.001). Using regression analysis, a 137-g decrease in birth weight was predicted (15). Statistical significance was also present when the data were categorized by sex (males 3561 g vs. 3733 g (p<0.05), females 3364 g vs. 3538 g (p<0.05)), percentage of infants less than 3000 g (15% vs. 9% (p<0.05)), and percentage of infants at or greater than 4000 g (12% vs. 23% (p<0.01)). Infant characteristics unrelated to the father's drinking were length, head circumference, gestational age, and Apgar scores (15). Consideration of the mother's drinking, smoking, and marijuana use did not change the statistical significance of the data. Nor could the differences be attributed to any of 20 reproductive and socioeconomic variables that were examined, including paternal smoking and marijuana use. No increases in structural defects were detected in the infants of the regular drinking fathers, but the sample size may have been too small to detect such an increase (14). In contrast to these data, other researchers have been unable to find an association between paternal drinking and infant birth weight (16). Thus, additional research is required, especially because the biologic mechanisms for the proposed association have not been determined (15).

The mechanism of ethanol's teratogenic effect is unknown but may be related to acetaldehyde, a metabolic byproduct of ethanol (7). One researcher reported higher blood levels of acetaldehyde in mothers of children with FAS than in alcoholics who delivered normal children (17). However, the analysis techniques used in that study have been questioned, and the high concentrations may have been due to artifactual formation of acetaldehyde (18). At the cellular level, alcohol or one of its metabolites may disrupt protein synthesis, resulting in cellular growth retardation with serious consequences for fetal brain development (19). Other proposed mechanisms that may contribute, as reviewed by Shepard (20), include poor protein intake, vitamin B deficiency, lead contamination of alcohol, and genetic predisposition. Of interest, metronidazole, a commonly used anti-infective agent, has been shown to markedly potentiate the fetotoxicity and teratogenicity of alcohol in mice (21). Human studies of this possible interaction have not been reported.

Complete FAS consists of abnormalities in three areas with a fourth area often involved: (a) craniofacial dysmorphology, (b) prenatal and antenatal growth deficiencies, (c) central nervous system dysfunction, and (d) various other abnormalities (7,8). Problems occurring in the latter area include cardiac and renogenital defects and hemangiomas in about one-half of the cases (3,4 and 5,22). Cardiac malformations were described in 43 patients (57%) in a series of 76 children with the FAS evaluated for 06 years (age: birth to 18 years) (23). Functional murmurs (12 cases, 16%) and ventricular septal defects (VSD) (20 patients, 26%) accounted for the majority of anomalies. Other cardiac lesions present, in descending order of frequency, were: double outlet right ventricle and pulmonary atresia, dextrocardia (with VSD), patent ductus arteriosus with secondary pulmonary hypertension, and cor pulmonale. Liver abnormalities have also been reported (24,25). Behavioral problems, including minimal brain dysfunction, are long-term effects of the FAS (1).

Ten-year follow-up of the original 11 children who were first diagnosed as having the FAS was reported in 1985 (25). Of the 11 children, two were dead, one was lost to follow-up, four had borderline intelligence with continued growth deficiency and were dysmorphic, and four had severe intelligence deficiency as well as growth deficiency and dysmorphic appearance. Moreover, the degree of growth deficiency and intellectual impairment was directly related to the degree of craniofacial abnormalities (25). In the eight children examined, height, weight, and head circumference were deficient, especially the latter two parameters. The authors concluded that the slow head growth after birth may explain why, in some cases, the FAS is not diagnosed until 912 months of age (25). Cardiac malformations originally observed in the infants, atrial septal defect (one), patent ductus arteriosus (one), and ventricular septal defect (six), had either resolved spontaneously or were no longer clinically significant. Three new features of the FAS were observed: dental malalignments, malocclusions, and eustachian tube dysfunction (associated with maxillary hypoplasia and leading to chronic serous otitis media) (25).

Fetal Alcohol Syndrome (2,3,4,5,6,7,8 and 9,11,12 and 13,22,23,24,25,26,27,28,29,30,31,32,33,34,35,36,37 and 38) Craniofacial Eyes: short palpebral fissures, ptosis, strabismus, epicanthal folds, myopia, microphthalmia, blepharophimosis Ears: poorly formed concha, posterior rotation, eustachian tube dysfunction Nose: short, upturned hypoplastic philtrum Mouth: prominent lateral palatine ridges, thinned upper vermilion, retrognathia in infancy, micrognathia or relative prognathia in adolescence, cleft lip or palate, small teeth with faulty enamel, Class III malocclusion, poor dental alignment Maxilla: hypoplastic Central nervous system Dysfunction demonstrated by mild to moderate retardation, microcephaly, poor coordination, hypotonia, irritability in infancy and hyperactivity in childhood Growth Prenatal (affecting body length more than weight) and postnatal deficiency (length, weight, and head circumference) Cardiac Murmurs, atrial septal defect, ventricular septal defect, great vessel anomalies, tetralogy of Fallot Renogenital Labial hypoplasia, hypospadias, renal defects Cutaneous Hemangiomas, hirsutism in infancy Skeletal Abnormal palmar creases, pectus excavatum, restriction of joint movement, nail hypoplasia, radioulnar synostosis, pectus carinatum, bifid xiphoid, Klippel-Feil anomaly, scoliosis Muscular Hernias of diaphragm, umbilicus or groin, diastasis recti A study published in 1987 found that craniofacial abnormalities were closely related to alcohol consumption in a dose-response manner (39). Although a distinct threshold was not defined, the data indicated that the consumption of more than six drinks (90 mL of ethanol) per day was clearly related to structural defects, with the critical period for alcohol-induced teratogenicity around the time of conception (39). A 1989 study that examined 595 live singleton births found a significant correlation between alcohol use in the first 2 months of pregnancy and intrauterine growth retardation and structural abnormalities (40). Analysis of alcohol use during the other periods of pregnancy did not show a significant association with these outcomes.

A prospective study conducted between 1974 and 1977 at the Kaiser-Permanente health maintenance organization in Northern California was conducted to determine whether light to moderate drinking during pregnancy was associated with congenital abnormalities (41). A total of 32,870 women met all of the criteria for enrollment in the study. Of the total study population, 15,460 (47%) used alcohol during pregnancy, 17,114 (52%) denied use, and 296 (1%) provided incomplete information on their drinking. Of those drinking, 14,502 (94%) averaged less than one drink/day, 793 (5%) drank one to two drinks/day, 127 (0.8%) consumed three to five drinks/day, and 38 (0.2%) drank six or more drinks/day. The total (major and minor) malformation rates were similar between nondrinkers and light (less than one drink/day) or moderate (one to two drinks/day) drinkers; 78.1/1000, 77.3/1000, and 83.2/1000, respectively. A significant trend (p=0.034) was found with increasing alcohol use and congenital malformations of the sex organs (e.g., absence or hypertrophy of the labia, clitoris, and vagina; defects of the ovaries, fallopian tubes, and uterus; hypoplastic or absent penis or scrotum; intersex and unspecified genital anomalies) (41). Rates per 1000 for defects of the sex organs in nondrinkers and the four drinking groups were 2.8, 2.6, 6.3, 7.9, and 26.3, respectively. Genitourinary malformations (i.e., cryptorchidism, hypospadias, and epispadias) also followed an increasing trend with rates per 1000 women of 27.2, 27.5, 31.5, 47.2, and 78.9 (p value for trend = 0.04), respectively. At the levels of alcohol consumption observed in the study, no increase in the other malformations commonly associated with the FAS was found with increasing alcohol use.

A strong association between moderate drinking (>30 mL of absolute alcohol twice per week) and 2nd trimester (1527 weeks) spontaneous abortions has been found (27,28). Alcohol consumption at this level may increase the risk of miscarriage by 24-fold, apparently by acting as an acute fetal toxin. Consumption of smaller amounts of alcohol, such as one drink (approximately 15 mL of absolute alcohol) per week, was not associated with an increased risk of miscarriage in a 1989 report (42).

Ethanol was once used to treat premature uterine contractions. In a retrospective analysis of women treated for premature labor between 19681973, 239 singleton pregnancies were identified (43). In 136, the women had received oral and/or IV ethanol, in addition to bed rest and oral b-mimetics. The remaining 103 women had been treated only with bed rest and oral b-mimetics. The alcohol group received an average of 38 g of ethanol/day for 234 days. In addition, 73 of these women continued to use oral alcohol at home as needed to arrest uterine contractions. Treatment with ethanol was begun at 12 weeks' gestation or less in 82 (60.3%) of the treated women. The mean birth weights of the alcohol-exposed and nonexposed infants were similar, 3385 g vs 3283 g, respectively. No significant differences were found between the groups in the number of infants who were small for gestational age (weight or length <10th percentile), birth length, fetal and neonatal deaths, and infants with anomalies. No relationship was found between ethanol dose and birth weight, length, or neonatal outcome. None of the exposed infants had features of the typical fetal alcohol syndrome. Psychomotor development (age to sit, walk, speak sentences of a few words, and read) and growth velocity were similar between the two groups. One of the infants whose mother had been treated with IV alcohol was growth retarded from birth to 14 years of age. Eight (6.1%) of 131 alcohol-exposed infants were considered to have problems in school (hyperactivity, carelessness) compared with 2 (2.0%) of 99 controls, but the difference was not significant. Other complications observed were aphasia and impaired hearing in 2 infants of the treated group and a third infant with blindness in the right eye (this infant was delivered at 27 weeks' gestation and the condition was thought to be due to oxygen therapy). The authors concluded that the alcohol treatment for threatened 1st or 2nd trimester abortions did not cause fetal damage (43). However, an earlier study concluded that adverse effects occurred after even short-term exposure (44). This conclusion was reached in an evaluation of 25 children 47 years of age whose mothers had been treated with alcohol infusions to prevent preterm labor (44). In comparison with matched controls, seven children born during or within 15 hours of termination of the infusion had significant pathology in developmental and personality evaluations.

Two reports have described neural tube defects in six infants exposed to heavy amounts of alcohol during early gestation (45,46). Lumbosacral meningomyelocele was observed in five of the newborns and anencephaly in one. One of the infants also had a dislocated hip and clubfeet (45).

A possible association between maternal drinking and clubfoot was proposed in a short 1985 report (47). Three of 43 infants, delivered from maternal alcoholics, had fetal talipes equinovarus (clubfoot), an incidence significantly greater than expected (p<0.00001).

Gastroschisis has been observed in dizygotic twins delivered from a mother who consumed 150180 mL of absolute ethanol/day during the first 10 weeks of gestation (48). Although an association could not be proven, the authors speculated that the defects resulted from the heavy alcohol ingestion.

A 1982 report described four offspring of alcoholic mothers with clinical and laboratory features of combined FAS and DiGeorge syndrome (49). Several characteristics of the two syndromes are similar, including craniofacial, cardiac, central nervous system, renal, and immune defects (49). Features not shared are hypoparathyroidism (part of DiGeorge syndrome) and skeletal anomalies (part of FAS). A possible causative relationship was suggested between maternal alcoholism and the DiGeorge syndrome.

An unusual chromosomal anomaly was discovered in a 2-year-old girl whose mother drank heavily during early gestation (50). The infant's karyotype revealed an isochromosome for the long arm of number 9: 46,XX,-9, i(9q). The infant had several characteristics of the FAS, including growth retardation. The relationship between the chromosomal defect and alcohol is unknown.

Prospective analysis of 31,604 pregnancies found that the percentage of newborns below the 10th percentile of weight for gestational age increased sharply as maternal alcohol intake increased (51). In comparison to nondrinkers, mean birth weight was reduced 14 g in those drinking less than one drink/day and 165 g in those drinking three to five drinks/day. The risk for growth retardation was markedly increased by the ingestion of one to two drinks each day. Other investigators discovered that women drinking more than 100 g of absolute alcohol/week at the time of conception had an increased risk of delivering a growth-retarded infant (52). The risk was twice that of women ingesting less than 50 g/week. Of special significance, the risk for growth retardation was not reduced if drinking was reduced later in pregnancy. However, a 1983 report found that if heavy drinkers reduced their consumption in midpregnancy, growth impairment was also reduced, although an increased incidence of congenital defects was still evident (53). Significantly smaller head circumferences have been measured in offspring of mothers who drank more than an average of 20 ml of alcohol/day compared to nondrinkers (54). In this same study, the incidence of major congenital anomalies in drinkers and nondrinkers was 1.2% vs none (54). These authors concluded that there was no safe level of alcohol consumption in pregnancy.

Alcohol ingestion has been shown to abolish fetal breathing (55). Eleven women, at 3740 weeks' gestation, were given 0.25 g/kg of ethanol. Within 30 minutes, fetal breathing movements were almost abolished and remained so for 3 hours. No effect on gross fetal body movements or fetal heart rate was observed. However, a 1986 report described four women admitted to a hospital because of marked alcohol intoxication (56). In each case, fetal heart rate tracings revealed no or poor variability and no reactivity to fetal movements or external stimuli. Because of suspected fetal distress, an emergency cesarean section was performed in one patient, but no signs of hypoxia were present in the healthy infant. In the remaining three women, normalization of the fetal heart rate patterns occurred within 1114 hours when the mothers became sober.

A study of the relationship between maternal alcohol ingestion and the risk of respiratory distress syndrome (RDS) in their infants was published in 1987 (57). Of the 531 infants in the study, 134 were delivered at a gestational age of 2836 weeks. The 134 mothers of these preterm infants were classified by the amount of alcohol they consumed per occasion into abstainers (N=58) (none), occasional (N=21) (less than 15 mL), social (N=15) (1530 mL), binge (N=12) (greater than 75 mL), and alcoholic (N=28). The incidence of RDS in the infants from the five groups was 44.8%, 38.1%, 26.7%, 16.7%, and 21.4%, respectively. The difference between abstainers and those frankly alcoholic was significant (p<0.05). Moreover, assuming equal intervals of alcohol intake among the five groups, the decrease in incidence of RDS with increasing alcohol intake was significant (p<0.02). Adjustment of the data for smoking, gestational age, birth weight, Apgar score, and sex of the infant did not change the findings. The authors concluded that chronic alcohol ingestion may have enhanced fetal lung maturation (57).

Neonatal alcohol withdrawal has been demonstrated in offspring of mothers ingesting a mean of 21 ounces (630 mL) of alcohol/week during pregnancy (58). In comparison to infants exposed to an equivalent amount of ethanol only during early gestation or to infants whose mothers never drank, the heavily exposed infants had significantly more withdrawal symptoms. No differences were found between the infants exposed only during early gestation and those never exposed. Electroencephalogram (EEG) testing of infants at 46 weeks of age indicated that the irritability and tremors may be due to a specific effect of ethanol on the fetal brain and not to withdrawal or prematurity (59). Persistent EEG hypersynchrony was observed in those infants delivered from mothers who drank more than 60 ml of alcohol/day during pregnancy. The EEG findings were found in the absence of dysmorphology and as a result, the authors suggested that this symptom should be added to the definition of the FAS (59).

Combined fetal alcohol and hydantoin syndromes have been described in several reports (60,61,62 and 63). The infants exhibited numerous similar features from exposure to alcohol and phenytoin. The possibility that the agents are also carcinogenic in utero has been suggested by the finding of ganglioneuroblastoma in a 35-month-old boy and Hodgkin's disease in a 45-month-old girl, both with the combined syndromes (see also Phenytoin) (61,62 and 63). Adrenal carcinoma in a 13-year-old girl with FAS has also been reported (64). These findings may be fortuitous, but long-term follow-up of children with the FAS is needed.

An unusual cause of FAS was described in 1981 (65). A woman consumed, throughout pregnancy, 480-840 mL/day of an over-the-counter cough preparation. Since the cough syrup contained 9.5% alcohol, the woman was ingesting 45.679.8 mL of ethanol/day. The infant had the typical facial features of the FAS, plus an umbilical hernia and hypoplastic labia. Irritability, tremors, and hypertonicity were also evident.

In summary, ethanol is a teratogen and its use during pregnancy, especially during the first 2 months after conception, is associated with significant risk to the fetus and newborn. Heavy maternal use is related to a spectrum of defects collectively termed the fetal alcohol syndrome. Even moderate use may be related to spontaneous abortions and to developmental and behavioral dysfunction in the infant. A safe level of maternal alcohol consumption has not been established (7,8,66). Based on practical considerations, the American Council on Science and Health recommends that pregnant women limit their alcohol consumption to no more than two drinks daily (1 ounce or 30 mL of absolute alcohol) (8). However, the safest course for women who are pregnant, or who are planning to become pregnant, is abstinence (7,66).

[*Risk Factor X if used in large amounts or for prolonged periods.]

Breast Feeding Summary

Although alcohol passes freely into breast milk, reaching concentrations approximating maternal serum levels, the effect on the infant has been considered insignificant except in rare cases or at very high concentrations (67). Recent research on the effects of chronic exposure of the nursing infant to alcohol in breast milk, however, should cause a reassessment of this position.

Chronic exposure to alcohol in breast milk was found to have an adverse effect on psychomotor development of breast feeding infants in a 1989 report (68). In this study, breast-fed was defined as a breast feeding child who received no more than 473 mL (16 ounces) of its nourishment in the form of supplemental feedings/day. Statistical methods were used to control for alcohol exposure during gestation. Of the 400 infants studied, 153 were breast-fed by mothers who were classified as heavier drinkers (i.e., an average daily consumption of 1 ounce of ethanol or about two drinks, or binge drinkers who consumed 2.5 ounces or more of ethanol on a single occasion). The population sampled was primarily white, well-educated, middle-class women who belonged to a health maintenance organization. The investigators measured the mental and psychomotor development of the infants at 1 year of age using the Bayley Scales of Infant Development. Mental development was unrelated to maternal drinking during breast feeding. In contrast, psychomotor development was adversely affected in a dose-response relation (p for linear trend, 0.006). The mean Psychomotor Development Index (PDI) of infants of mothers who had at least one drink daily was 98, compared to 103 for infants of mothers consuming less alcohol (p<0.01). The decrease in PDI was even greater if only those women not supplementing breast feeding were considered. Regression analysis predicted that the PDI of totally breast-fed infants of mothers who consumed an average of two drinks daily would decrease by 7.5 points. These associations persisted even after more than 100 potentially confounding variables, including maternal tobacco, marijuana, and heavy caffeine exposures, were controlled for during pregnancy and the first 3 months after delivery. The authors cautioned that their findings were only suggestive and should not be extrapolated to other patient populations because of the relative homogeneity of their sample (68). Although the conclusions of this study have been criticized and defended (69,70), judgment on the risks to the nursing infant from alcohol in milk must be withheld until additional research has been completed.

The toxic metabolite of ethanol, acetaldehyde, apparently does not pass into milk even though considerable levels can be measured in the mother's blood (71). One report calculated the amount of alcohol received in a single feeding from a mother with a blood concentration of 100 mg/dL (equivalent to a heavy, habitual drinker) as 164 mg, an insignificant amount (72). Maternal blood alcohol levels have to reach 300 mg/dL before mild sedation might be seen in the baby. However, a 1937 report described a case of alcohol poisoning in an 8-day-old breast-fed infant whose mother drank an entire bottle (750 mL) of port wine (73). Symptoms in the child included deep sleep, no response to painful stimuli, abnormal reflexes, and weakly reactive pupils. Alcohol was detected in the infant's blood. The child made an apparently uneventful recovery.

Potentiation of severe hypoprothrombic bleeding, a pseudo-Cushing syndrome, and an effect on the milk-ejecting reflex have been reported in nursing infants of alcoholic mothers (74,75 and 76). The American Academy of Pediatrics considers maternal ethanol use to be compatible with breast feeding, although it is recognized that adverse effects may occur (77).

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Questions and Answers

ethanol????????????????, say i have 2 different plants 1 of them is more ideal for making ethanol than the other, i make ethanol out of moth plants. Would the amount of ethanol made be the same just different concentrations or would different amounts be made?

you will get different amounts. for example lets take sugar cane and corn plants for instance. with sugar cane you need 100lbs to get a yield of 11 gallons of ethanol. with corn you need over 200lbs to get the same yield. this yield is fuel quality ethanol, NOT the total yield. fuel quality ethanol needs ot be at least 160 proof.

What percentage denatured ethanol is usually used as a solvent for food in general?, I'm using it for a science fair project but I'm not sure whether to buy 70% ethanol or 99% ethanol--the only types found at Superstore last time I checked. My teacher only told me that I can get it from basically any grocery store or drug store. Please help! Thank-you.

I've never quite heard of ethanol used as a solvent for food.

However, I know that 70%-75% ethanol is used for simple sterilization in biology laboratories. Like to spray on gloved hands after working with cells.

What is the Difference between Denatured ethanol and Absolute Ethanol?, What is the Difference between Denatured ethanol and Absolute Ethanol?

Also what is the uses of each one?

Thank you,

Denatured alcohol has one or more substances added to it to prevent it from being used for drinking. This type of alcohol is for solvent/industrial use. It could be used in a chemical laboratory, if the additives don't interfere with your reactions.

Absolute alcohol is anhydrous alcohol for use in a chemical laboratory etc. Since they often dry the alcohol by addition of benzene and then distilling off the ternerary azeotrope (alcohol/water/benzene) it might still contain a little benzene. Sometimes they use other drying methods, however.

Supposedly the 95% ethanol (95% ethanol/5% water) is the one that could be drunk, but I am not absolutely certain. I would suggest you spend the extra money to get real liquor if that is your ulterior motive.

PS: I would NEVER drink the punch at chemistry dept. parties because I never knew what grade of alcohol some idiot might have spiked the punch with.

What is it in ethanol (the elements that make up ethanol) that makes ethanol a depressant?, Ethanol is classified for medical purposes as a central nervous system depressant. What is it in ethanol, its chemical structure or the elements found in ethanol, that reacts with the central nervous system that makes it a depressant?

ethanol consists of ethane n alcohol.its common name is ethyl alcohol n it's an alcohol.

How to protect from Ethanol Phase Separation in Bertram Fiberglass Gas Tanks with E-10 Gasoline?, Hi, I have a 1985 Bertram 30 with a 220 Gallon Fiberglass Tank. As we approach the end of the season in the Northeast, we now have to start planning for Winterization. A standard procedure for Winterization over the years was to fill up your tanks with Gasoline before winter storage to cut down on water/condensation. That was before this Ethanol fiasco! Now if we have phase separation in the E-10 Gas, the Ethanol can eat away at the fiberglass resin in the tanks and also leave deposits in the Heads of the engine.

I have been treating the fuel with Startron for the past year.

What should I do this Winter? Should I fill up the tank with Startron treated fuel or should I leave 1/2 or even less than of tank of Startron treated fuel?

You have 2 choices really. You can fill it up and treat it or you should empty it entirely and run your engine out of gas also. If you leave it any other way you invite trouble. Ethanol will pull moisture out of the air and into the tank also giving you troubles. We have had ethanol for a few years in the northeast now so if you have not had trouble yet you should be fine leaving it full and treating it. Good luck.

How does adding ethanol effect the octane rating of gasoline?, Would it be helpful to put a gallon of ethanol in my tank each time I fill up?

You be the judge... Ethanol burns very hot and is not prone to preignition..... common to high octane numbers.... which is the ability to withstand higher compressions without knocking due to preignition.

E85 has an octane rating of 105 (compared to 89-93 for normal US gasolines) and ethanol by itself is rated at 116....

Most "octane boosters" are made of toluene or ethanol or xylene.....

Using a gasoline with too high an octane can cause stalling when cold and possible valve damage due to not seating to transfer heat.

A gallon of ethanol per 12-20 gallons should be fine. Back in the 'old' days we used to have this stuff called gasohol that was 5 to 10 percent ethanol or methanol (Carter started it during the fuel crunch, funny how we forget the past, to stretch US supplies of oil and gasoline). Don't use methanol though, if the fuel system is not designed for it, it will eat the rubber and polymer fuel lines.

What is the physical state of ethanol at room temperature?, Ethanol melts a -114.1 degrees celcius and boils at 78.5 degrees celcius. What is the physical state of ethanol at room temperature?

Ethanol is in liquid state at room temperature. Normal room temperature never goes up (even in the hottest places) more than the boiling point of ethanol. And the lowest temperature would not be so low either for ethanol to freeze. So ethanol exists as liquid at room temperature.
I hope you know that boiling point means the temperature at which ethanol evaporates and escapes as gas.

Hope it helped!

What is the molarity of ethanol in a vermouth drink, if the vermouth is 36 proof?, A solution that is 95% ethanol is 190 proof. What is the molarity of ethanol in a vermouth drink, if the vermouth is 36 proof? The density of ethanol is 0.78 g/mL

For 36 proof I figured its 18%. I got an answer of 3.05 M of ethanol, but I'm not sure.

36 proof = 18% ethanol = 18g ethanol/100mL vermouth

Atomic weights: C=12 H=1 O=16 C2H5OH=46

Let ethanol be called E. Let vermouth be called V.

18gE/100mLV x 1molE/46gE x 1000mLV/1LV = 3.9 mole/L

What conditions are required for ethanol to react with ethanoic acid?, For the reaction between ethanol and ethanoic acid:

1. What catalyst is used?

2. What are the reaction conditions?

What does the compostion of ethanol and water have to do with the reason for ethanol boiling first?, if that makes sense, where it has to do with the hydrogen bonding and the polar/nonpolar ends that make the ethanol vaporize before the water.

other wise. why does ethanol have a lover boiling point than water?

ethanol is not as polar as water.
Water is an extremely polar molecule, this is often described by the hydrogen bonds present in water. This causes there to be strong intermolecular forces.

Since the intermolecular forces of water are much stronger than those of ethanol, it causes water to stay in the liquid form for longer.

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