Evaluation in vinyl chloride monomer (VCM)-exposed workers and the relationship between liver lesions and gene polymorphisms of metabolic enzymes

Table 1 Prevalence of symptoms and signs between exposure and control groups

0.42 (0.20-0.88)Symptoms and signs	Exposure group )	Control group	Relative risk (RR
	n = 238(%)	n = 212(%)
Neurastheniaa	40 (16.81)	21 (9.91)	1.74 (1.06-2.58)
Pharyngeal irritationb	138 (57.98)	63 (29.72)	1.97 (1.56-2.48)
Abnormal ECGa	24 (10.08)	40 (18.87)	0.51 (0.32-0.83)
Cholelithiasis	6 (2.52)	7 (3.30)	0.76 (0.26-2.24)
Renal cyst	2 (0.84)	3 (1.42)	0.59 (0.10-3.52)
Liver ultrasonography abnormalityb	51 (21.41)	5 (2.36)	10.69 (4.38-26.12)
Fatty livera	10 (4.20)	21 (9.91)	0.42 (0.20-0.88)
Hemoglobin disordersa	46 (19.33)	22 (10.38)	2.07 (1.20-3.57)
Hypertension	11 (4.62)	15 (7.07)	0.64 (0.29-1.42)
Hepatic hemangioma	3 (1.26)	3 (1.42)	0.89 (0.18-4.37)
Leucopenia	4 (1.68)	1 (0.47)	3.61 (0.40-32.53)

^aP < 0.05 vs control group;

^bP < 0.01 vs control group.

Table 2 Prevalence of symptoms and signs among VCM-exposed workers stratified by VCM exposure

Symptoms and signs	VCM exposure
	≤ 15 000 mg		> 15 000 mg		Total
	(n = 186)		(n = 52)		(n = 238)
Neurastheniaa	26	14.00%	14	26.92%	40	16.81%
Respiratory system	3	1.60%	1	1.92%	4	1.68%
Digestive system	4	2.15%	1	1.92%	5	2.10%
Pharyngitisa	104	55.90%	34	65.38%	138	57.98%
ECG	19	10.20%	5	9.61%	24	10.08%
Nephridium USG	1	0.53%	2	3.85%	3	1.26%
Gall bladder USG	4	2.15%	4	7.69%	8	3.36%
Liver USGa	34	18.30%	17	32.69%	51	21.43%
Fatty liver	7	3.76%	3	5.77%	10	4.20%
Hepatic hemangioma	1	0.53%	2	3.85%	3	1.26%
Splenomegaly	8	4.30%	2	3.85%	10	7.08%

^aP < 0.05 vs ≤ 15 000 mg group.

Table 3 Liver lesions status according to genotypes and variables of interest in VCM exposure group

	VCM exposure group		Adjusted OR (95%CI)
	Control(n = 58)	Liver lesions(n = 58)
GSTT1
Non-null	31 (53.4%)	37 (63.8%)	1.0 (reference)
Null 27	(46.6%)	21 (36.2%)	0.65 (0.31-1.37)
GSTM1
Non-null	37 (63.8%)	36 (62.1%)	1.0 (reference)
Null	21 (36.2%)	22 (37.9%)	1.08 (0.51-2.29)
CYP2E1
c1c1	43 (74.1%)	27 (46.6%)	1.0 (reference)
c1c2/ c2c2	13/2 (25.8%)	24/7 (53.4%)	3.29 (1.51-7.20) b
ALDH2
1-1	37 (63.8%)	36 (62.1%)	1.0 (reference)
1-2/2-2	17/4 (36.2%)	17/5 (37.9%)	1.08 (0.51-2.29)
ADH2
1-1	4 (6.9%)	9 (15.5%)	1.0 (reference)
1-2/2-2	24/30 (93.1%)	22/27 (84.5%)	0.40 (0.12-1.39)
Age (yr)
< 35	41 (70.7%)	35 (60.3%)	1.0 (reference)
≥ 35	17 (29.3%)	23 (46.6)	2.10 (0.76-3.43)
Drinking
No	53 (91.4%)	47 (81.0%)	1.0 (reference)
Yes	5 (9.6%)	11 (19.0%)	2.48 (0.80-7.66)
Smoking
No	40 (69.0%)	41 (71.7%)	1.0 (reference)
Yes	18 (31.0%)	17 (29.3%)	0.92 (0.42-2.04)

^bP < 0.01 vs control.

Table 4 ORs for analysis of correlation between exposure and genotypes

Genotypes	Cumulative VCM exposure
	≤ 15 000 mg			> 15 000 mg
	Control	Liver lesion	OR (95% CI)	Control	Liver lesion	OR (95% CI)
GSTT1
Null	15	23	1	16	14	1
GSTM1	17	9	0.3 (0.1-0.9)a	10	12	1.4 (0.5-4.1)
GSTM1
Non-null	21	21	1	16	15	1
Null	11	11	1.0 (0.4-2.8)	10	11	1.2 (0.4-3.6)
CYP2E1
c1c1	23	16	1	20	11	1
c1c2/ c2c2	9	16	2.6 (0.9-7.2)	6	15	4.6 (1.4-15.1)a
ALDH2
1-1	20	22	1	17	14	1
1-2/2-2	12	10	0.8 (0.3-2.1)	9	12	1.6 (0.5-5.0)
ADH2
1-1	2	8	1	2	1	1
1-2/2-2	30	24	0.2 (0.1-1.0)a	24	23	2.1 (0.2-24.5)

^aP < 0.05 vs≤ 15 000 mg group.

Table 5 Logistic regression analysis of liver lesions

	Logistic regression analysis
	Coefficient	P	OR (95% CI)
Age (yr)	0.47	0.33	1.60 (0.62-4.19)
Duration of work	0.24	0.60	1.27 (0.52-3.12)
Drinking	1.14	0.10	3.14 (0.78-12.64)
Smoking	-0.9	0.13	0.41 (0.13-1.29)
Gender	-0.06	0.91	0.94 (0.36-2.47)
GSTT1	-0.51	0.23	0.60 (0.26-1.39)
GSTM1	-0.15	0.75	0.86 (0.36-2.10)
CYP2E1	1.16	0.009b	3.17 (1.33-7.57)
ALDH2	0.09	0.84	1.09 (0.46-2.58)
ADH2	-0.72	0.31	0.49 (0.12-1.96)
Constant	0.24	0.84

^bP<0.01 vs control.