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Table 2 Distribution of CYP1A1, EPHX, and GSTM1 genotypes in exposed and control subjects. Data are reported as the number of subjects (percentage between brackets).

From: Primary DNA damage and genetic polymorphisms for CYP1A1, EPHX and GSTM1 in workers at a graphite electrode manufacturing plant

Genotype Exposed workers Controlsa
CYP1A1 (MspI)b w1/w1 79 (72.5) 67 (83.8)
w1/m1 + m1/m1 30 (27.5) 13 (16.3)
CYP1A1 (Ile/Val)c w2/w2 98 (89.9) 73 (91.3)
w2/m2 + m2/m2 11 (10.1) 7 (8.8)
EPHX d Low 59 (54.1) 35 (43.8)
   Medium + High 50 (45.9) 45 (56.3)
GSTM1 Active 63 (57.8) 44 (55.0)
   Null 46 (42.2) 36 (45.0)
  1. a Two control subjects were not genotyped.
  2. b w1 = common allele, m1 = variant allele.
  3. c w2 = common allele; m2 = variant allele.
  4. d mEH-deduced activity. The mEH activity deduction was based on the results of genotyping of polymorphisms in exons 3 and 4: subjects carrier of combination (exons 3 and 4) His113His + His139His, His113His + His139Arg, or Tyr113His + His139His, were considered as having "low" activity of mEH; subjects carrier of combination (exons 3 and 4) Tyr113Tyr + His139His, Tyr113His + His139Arg, or His113His + Arg139Arg, were considered as having "medium" activity of mEH; subjects carrier of combination (exons 3 and 4) Tyr113Tyr + His139Arg, Tyr113Tyr + Arg139Arg, or Tyr113His + Arg139Arg, were considered as having "high" activity of mEH [31].
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BMC Public Health

ISSN: 1471-2458

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