Table 1 Association between smoking behaviour and nicotine dependence and ANKK1 / DRD2 Taq IA, SLC6A3 VNTR, and CYP2A6 polymorphisms

Noble et al. (1994)

Caucasians

57 current smokers, 115 former smokers, and 182 non-smokers

Smoking subjects showed a significantly higher prevalence of the A1 allele compared to controls. Both past and current smokers demonstrated a significantly higher prevalence of the A1 allele than non-smokers did.

[4]

Comings et al. (1996)

Caucasians

312 smokers

There was a significant, inverse relationship between the prevalence of the A1 allele and the age of onset of smoking, and the maximum duration of time that smokers had been able to quit smoking on their own.

[5]

Batra et al. (2000)

Caucasians

110 heavy smokers and 60 light smokers

No significant findings

[22]

Bierut et al. (2000)

Caucasians

388 habitual smokers and 566 non-habitual smokers

No significant findings

[23]

Yoshida et al. (2001)

Japanese

77 current smokers, 57 former smokers, and 198 never smokers

Smoking appeared to be associated with the A2/A2 genotype.

[6]

Hamajima et al, (2002)

Japanese

226 current smokers, 133 former smokers, and 434 never smokers

Males with the A2/A2 genotype had a higher risk of being current smokers.

[7]

Johnstone et al. (2004)

Caucasians

752 smokers

At 1 week, the nicotine patch was more effective for smokers with the A1/A2 or A1/A1 genotypes than for those with the A2/A2 genotype; this was not the case at the 12-week flow up.

[24]

Morton et al. (2006)

Caucasians

1068 smokers, 213 non-smoking, and 1093 former smokers

Current smokers were more likely than former smokers to possess the A1 allele.

[25]

Connor et al. (2007)

Caucasians

84 smokers

Compared to carriers of the A2/A2 genotype, carriers of the A1/A1 or A1/A2 genotypes were characterised by higher levels of cigarette consumption.

[26]

Lerman et al. (1999)

Caucasians (85%) African Americans (15%)

289 smokers and 233 non-smokers

Individuals with the 9r allele were significantly less likely to be smokers, particularly if they also carried the A2/A2 genotype. Smokers carrying the 9r allele genotype were also significantly less likely to have started smoking before 16 years of age and had prior smoking histories, indicating a longer period of prior smoking cessation.

[10]

Sabol et al. (1999)

Caucasians

164 current smokers and 111 former smokers

The 9r allele was associated with smoking cessation.

[11]

Jorm et al. (2000)

Caucasians

211 former smokers, 198 current smokers, and 452 non-smokers

No associations were found with either smoking initiation or smoking cessation.

[12]

Vandenbergh et al. (2002)

Caucasians

153 former smokers, 98 current smokers, 214 never smokers, and 114 non-smokers

Never smokers showed a higher prevalence of the 10r allele compared to current smokers. The frequency of the 10r allele in never-smokers (no cigarettes ever) was more than that in other smokers.

[13]

Perkins et al. (2008)

Caucasians

72 smoker

The increase in smoking amount owing to negative mood was associated with the A2/A2 allele and the 9r allele.

[17]

Laucht et al. (2008)

Caucasians

220 ever smokers (adolescents)

The A1 allele scored higher on nicotine dependence than their allelic counterparts. The intention to quit smoking was significantly lower in adolescents for the 10r/10r genotype.

[27]

Sieminska et al. (2009)

Caucasians

150 ever smokers and 158 never smokers

The abstinence periods during quitting attempts of carriers of the A1 allele were longer than those of non-carriers. The odds ratio for heavy smoking was higher in carriers of the A1 or 9r alleles compared to that in non-carriers. Compared to non-carriers, carriers of the 9r allele had a lower risk to start smoking before the age of 20 years.

[14]

Tan et al. (2001)

Chinese

174 smokers and 152 non-smokers

The distribution of the CYP2A6 genotype frequencies was not significantly different.

[28]

Loriot et al. (2001)

Caucasians

185 heavy smokers and 203 light smokers

No significant relationship between genetically impaired nicotine metabolism and cigarette consumption related and the presence of defective CYP2A6 alleles (*2 and *4 alleles).

[29]

Ando et al. ( 2003)

Japanese

57 current smokers, 44 former smokers, and 139 never smokers

The proportion of never smokers among heterozygous carriers of the *4 allele was similar among subjects with the *1/*1 genotype. CYP2A6 genotypes did not correlate either with the number of cigarettes smoked per day or with the age of smoking commencement.

[30]

Minematsu et al. (2003)

Japanese

92 current smokers, 111 former smokers, and 123 non-smoker

The percentage of subjects with a CYP2A6del (*4) allele was lower among heavy smokers than among light smokers or non-smokers and was lower among ex-smokers than among current smokers.

[20]

Fujieda et al. (2004)

Japanese

1094 patient (cancer) subjects and 611 healthy subjects

The amount of daily cigarette consumption in subjects who harboured the CYP2A6*4 allele was significantly less than that in subjects carrying the *1/*1 genotype.

[31]

Kubota et al. (2006)

Japanese

107 smokers

CYP2A6 high-activity group (CYP2A6*1/*1, *1/*4, etc.) smoked the first cigarette of the day earlier than the low-activity group (CYP2A6*4/*4), indicating more marked nicotine dependence. Nicotine withdrawal symptoms were more serious during smoking cessation in the CYP2A6 high-activity group.

[21]

Liu et al. (2011)

Chinese

970 current smokers and 358 former smokers

Poor metabolizers reported smoking fewer cigarettes per day, started smoking regularly at a later age, and smoked for a shorter duration than did normal metabolizers. However, poor metabolizers were less likely to quit smoking than normal metabolizers were.

[32]