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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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