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. 2015 Jul 27;16(8):17029–17047. doi: 10.3390/ijms160817029

Table 3.

Oral cancer risk and alcohol drinking.

Reference Type of Article Wine * Oral Cancer Risk
[11] Meta-analysis No Oral and pharyngeal cancer RR 1 = 5.13 for heavy drinkers.
[59] Meta-analysis No Upper aero-digestive tract cancer: RR = 2.97 (but RR = 2.24 only considering oral cavity, pharynx, and larynx); alcohol intake increasing of 10 g/day equivalent to increasing RR of 1.09.
[26] Meta-analysis Yes Wine-specific RR = 2.1 for any drinking pattern; RR = 4.92 for heavy drinking (≥4 drinks/day).
[27] Meta-analysis No RR = 1.05 for light drinkers.
[13] Meta-analysis No 25% Alcohol-attributable cases for upper aero-digestive tract cancer.
[12] Meta-analysis No 30% Alcohol-attributable cases for oral cavity and pharynx cancer with an increased risk related to 1 g/day of ethanol of 0.0185%.
[26] Meta-analysis No RR = 1.3 for 10 g/day, 3.2 for 50 g/day, 8.6 for 100 g/day and 13.0 for 125 g/day of ethanol.
[60] Meta-analysis No RR = 1.1 for light drinkers; RR = 4.6 for heavy drinkers.
[8] Meta-analysis No Oral cancer RR = 1.65 for 1–39 g/day of ethanol in men; RR = 1.43 for 1–19 g/day in women.
[61] Meta-analysis No Oral cancer RRs = 1.86, 3.11 and 6.45 for ethanol intake of 25, 50 and 100 g/day, respectively.
[62] Meta-analysis No Oral cavity and pharynx cancers RRs = 1.75 (25 g/day of ethanol), 2.85 (50 g/day), 6.01 (100 g/day).
[63] Meta-analysis No Oral cancer RRs = 2.2, 4.2 and 10.7 for ethanol intake of 25, 50 and 100 g/day, respectively.
[64] Cohort study (Netherlands) No Oral cavity cancer: RRs = 1.25, 1.91, 3.88, 6.39 for 0–5, 5–15, 15–30, ≥30 g/day of ethanol; for regular consumers: RRs = 1.65, 1.68, 3.20, 7.50 in the same order; wine specific: RR = 1.07, 1.31, 0.93, for intake of 0–1, 1–2, ≥2 glasses/day.
[30] Cohort study (Korea) No Daily binge drinkers versus non binge-drinkers: oropharyngeal cancer mortality HR 2 = 4.82; adjusting for the volume of alcohol intake and frequency of binge, HR = 4.90.
[65] Case-control (Brazil) No Drinking was not independently associated with oral cancer; drinking status: ever drinker OR 3 = 4.21, level-1 drinker (≤862 g/year) OR = 1.68, level-2 drinker (>862 g/years) OR = 6.73; drinking and smoking status: never smoker and ever drinker OR = 0.58, ever smoker and ever drinker OR = 5.85.
[4] Case-control ICARE study (France) No Population-attributable risk of oral cavity cancer 7.3% for alcohol drinking.
[7] Case-control ARCAGE multi-centre study (10 European countries) No Oral cancer OR = 1.04 related to alcohol alone; OR = 7.06 related to alcohol/smoking joint effect.
[66] Case-control (Turkey) Yes Oral cancer OR = 0.549 for red wine intake.
[28] Ecological study (Europe, North America, Oceania and Far Eastern Asia) Yes Male age-standardised mortality rate for oral cancer: significantly increasing for every litre of pure ethanol (0.15 per 100,000 subjects) and spirits (0.26 per 100,000 subjects), but non-significant effects for beer and wine.
[67] Case-control (4 European countries, Cuba, Canada, India, Sudan and Australia) Yes ORs = 2.86 for ever drinker, 2.12 for ex-drinkers, 3.46 for current drinkers; type of drink: only beer OR = 1.16, only wine and beer OR = 1.96, only wine OR = 2.71, spirits with or without wine or beer OR = 7.28; drinking amount (independently from type of beverage): for 1 drink/day OR = 2.00, for 2 drinks/day OR = 3.74, for 3–4 drink/day, OR = 6.22, for 5–6 drink/day OR = 10.58, for 7–10 drink/day OR = 10.29.
[68] Case-control (Italy and Switzerland) Yes Wine, OR = 1.0 for 1–2 drinks/day, 2.2 for ≥3 drinks/day.
[69] Case-control (Southern Greece) Yes OR = 1.7 for moderate drinkers (1–28 drinks/week); ORs = 0.8 and 1.1 only considering wine drinkers of 1 drinks/week and ≥14 drinks/week, respectively.
[70] Case-control (Spain) Yes OR = 1.89 for 1–50 g/day of alcohol; OR = 5.3 in wine drinkers exceeding 50 g/day of ethanol (i.e., 4 glasses per day).
[6] Cohort study (Denmark) Yes RR = 3.0 for drinkers of 7–21 beers or spirits/week, but not wine, compared with non-drinkers; RR = 0.5 for subjects with the same total alcohol intake, but with wine (>30% of their intake); RR = 5.2 for drinkers of >21 beers and spirits/week but not wine, RR = 1.7 for subjects with the same total alcohol intake, but including wine.
[71] Case-control (Japan) No OR = 3.6, 4.5 and 4.8 for sake, beer and hard liquor drinkers, respectively.
[72] Case-control (Italy) Yes OR = 11.2, 9.9 and 4.1 among heavy drinkers (≥84 drinks/week) of wine only, wine and spirits and combination wine-spirits-beer.
[73] Case-control (North Italy) Yes OR = 4.9 for heavy wine drinkers (≥56 glasses/week, i.e., about 1 litre/day), rising to 8.5 for drinkers of ≥84 glasses/week.
[49] Salivary biokinetics (Caucasoid healthy subjects) Yes Acute intake of 125 mL of red wine: no effect on anti-radical salivary capacity, but administration of red wine polyphenol capsules improved the salivary antioxidant status.
[52] Salivary and blood biokinetics (Asian healthy subjects) Yes Acute intake of 0.6 g ethanol/kg body weight in the form of 13% ethanol Calvados, 13% ethanol shochu, 13% ethanol red wine and 5% ethanol beer.
[74] Salivary and blood biokinetics (Asian heavy drinkers-alcoholics) No Patients with homozygous alcohol dehydrogenase-1B (ADH1B*1/*1), who drunk the day before, were associated with higher levels of ethanol persisting in the blood for longer periods and had higher salivary acetaldehyde levels, correlating to oral bacteria and yeast counts; no effect of inactive heterozygous aldehyde dehydrogenase-2 (ALDH2*1/*2) was observed on ethanol lingering the next morning.
[75] Salivary and blood biokinetics (Asian healthy subjects) No Acute intake of 0.4 g ethanol/kg body weight in a standardized 10% (v/v) solution of absolute ethanol in orange juice (with and without previous ingestion of 4-methylpyrazole, an inhibitor of human ADH): a high salivary production of acetaldehyde by oral microflora alcohol dehydrogenase was observed.
[55] Salivary and blood biokinetics (Asian and Caucasoid healthy subjects) No Acute intake of 0.5 g ethanol/kg body weight in a standardized 10% (v/v) solution of absolute ethanol in orange juice: Aldehyde dehydrogenase-2 (ALDH2) deficient subjects had 2–3 times higher salivary acetaldehyde levels than ones with normal ALDH2, after 240 min; salivary acetaldehyde originated from oral microflora and parotid gland ethanol metabolism.
[54] Salivary and blood biokinetics/cohort study (Finland, healthy subjects, dental and oral cancer patients, heavy drinkers—alcoholics) No Smoking and heavy alcohol intake increased salivary acetaldehyde; considering alcoholic status, levels of acetaldehyde were: teetotalers 111 μmol/L, moderate alcohol consumption 104 μmol/L, heavy drinkers 172 μmol/L.
[76] Salivary and blood biokinetics (Caucasoid healthy subjects) No Acute intake of 0.5 g ethanol/kg body weight in a standardized 10% (v/v) solution of absolute ethanol in orange juice; salivary acetaldehyde was associated with oral microflora: it peaked within 40 min after ethanol ingestion and decreased after a 3-day use of antiseptic mouthwash (chlorhexidine).

* Wine-specific analysis of data for oral cancer risk; 1 RR, relative risk; 2 HR, hazard ratio; 3 OR, odd ratio.