Chronic cigarette smoking is associated with diminished folate status, altered folate form distribution, and increased genetic damage in the buccal mucosa of healthy adults.
BACKGROUND
Smoking causes genetic damage in buccal cells and increases the risk of oral cancer. Because folate is instrumental in DNA synthesis and repair, it is a determinant of genetic stability and therefore might attenuate the genotoxic effects of smoking.


OBJECTIVE
Our aim was to compare the presence of folate metabolites and select indicators of genetic damage in the mouths of chronic smokers and nonsmokers.


METHODS
Dietary, biochemical, and molecular correlates of folate status were measured in healthy smoker (n = 35) and nonsmoker (n = 21) groups of comparable age, sex, and body mass indexes.


RESULTS
After correction for dietary intake, the smokers displayed lower plasma, erythrocyte, and buccal mucosal cell (BMC) folate (20%, 32%, and 50% lower, respectively; P < 0.05) and lower plasma vitamin B-12 and pyridoxal 5-phosphate (P < 0.05) than did nonsmokers. Folate in the BMCs of smokers comprised significantly greater proportions of pteroylmonoglutamate, formyltetrahydrofolate, and 5,10-methenyltetrahyrofolate than did folate in the BMCs of nonsmokers. Although the degree of genomic methylation and uracil incorporation in the buccal cells of the 2 groups were not significantly different, the BMC micronucleus index, a cytologic indicator of genetic damage, in the smokers was 2-fold that of the nonsmokers (9.57 compared with 4.44 micronuclei/1000 cells; P < 0.0001). Neither systemic nor oral folate status was an independent predictor of micronuclei.


CONCLUSIONS
Chronic smoking is associated with a lower systemic status of several B vitamins, reduced oral folate, and changes in folate form distribution in the mouth. However, the cytologic damage that is evident in the mouths of smokers does not correlate with oral folate status.
Gabriel
Helen E
HE
Vitamins and Carcinogenesis Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, 711 Washington Street, Boston, MA 02111, USA.
Crott
Jimmy W
JW
Ghandour
Haifa
H
Dallal
Gerard E
GE
Choi
Sang-Woon
SW
Keyes
Mary K
MK
Jang
Hyeran
H
Liu
Zhenhua
Z
Nadeau
Marie
M
Johnston
Abbey
A
Mager
Donna
D
Mason
Joel B
JB
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D016022:Case-Control Studies; D002869:Chromosome Aberrations; D004247:DNA / Q000378:metabolism*; D004912:Erythrocytes / Q000737:chemistry; D005260:Female; D005492:Folic Acid / Q000097:blood / Q000737:chemistry / Q000378:metabolism*; D006801:Humans; D008297:Male; D015162:Micronucleus Tests; D008875:Middle Aged; D009061:Mouth Mucosa / Q000166:cytology / Q000473:pathology*; D009752:Nutritional Status; D011732:Pyridoxal Phosphate / Q000097:blood; D012907:Smoking / Q000009:adverse effects* / Q000097:blood / Q000378:metabolism; D014803:Vitamin B Complex / Q000097:blood
D014803:Vitamin B Complex; D011732:Pyridoxal Phosphate; D004247:DNA; D005492:Folic Acid