OCCUPATIONAL EXPOSURE TO ARSENIC

1
OCCUPATIONAL EXPOSURE TO ARSENIC COMPOUNDS
BIOMONITORING OF GENOTOXIC EFFECTS
Mateuca Raluca1, Carton Christian2, Aka Peter1
and Kirsch-Volders Micheline1
1Vrije Universiteit Brussel (V.U.B.),
Laboratorium voor Cellulaire Genetica, Pleinlaan
2, B-1050 Brussels, Belgium (email
rmateuca_at_vub.ac.be) 2 Service of Occupational
Health, Belgian Defence, Belgium (email
Christian.Carton _at_mil.be)
MATERIALS AND METHODS
INTRODUCTION
Micronucleus (MN) test
Mechanisms of As (III) induced genotoxicity (4)
(5)
Arsenic is an established human carcinogen (Group
1) causing lung tumors by inhalation and cancers
of the skin and bladder by ingestion (1).
However, the underlying mechanisms of arsenic
carcinogenicity are still not fully understood.
Biologically, the trivalent sodium arsenite is
significantly more active than the pentavalent
sodium arsenite (2). Many epidemiological studies
reported increased incidences of chromosomal
aberrarions (CAs), sister chromatid exchanges
(SCE) and micronuclei (MN) in human populations
exposed to arsenic through drinking water (1)(3).
Sister chromatid exchage (SCE) test
Chromosomal aberration test (CAs)
STUDY DESIGN
The study comprised three groups of workers 19
protected plant workers (NIOSH level B
protection) regularly exposed to arsenic
compounds at a mean level above the current
TLV-TWA (10 µg As/m3)(Group 1), 16 non-protected
field workers accidentally exposed to arsenic
(Group 2) and a third group of 21 matched office
employees as controls.
Statistics t-test, Mann-Whitney U test,
multiple regression analysis
RESULTS
OBJECTIVES

• To evaluate cytogenetic damage as measured by the
  frequencies of SCE, high frequency cells (HFC),
  micronuclei (MNCB and MNMC) and CAs in workers
  exposed to arsenic compounds.
• To improve protection at the population and
  individual level.

Table 1 Characteristics of the study population
Table 2. Significant genotoxicity parameters in
all workers (n 56)
Significance level in the model. Values in bold
are p-values for each of the predictor variables.
Fig.1. Comparison between urinary As levels in
plant and field exposed workers
Fig. 2. Increased genotoxicity parameters in
plant exposed workers (Group 1)
Fig. 3. Increased genotoxicity parameters in
exposed smokers
40
5.0
P 0,016
P 0,028
30
2.5
Cells with CAs
20
HFC
10
0.0
0
Exposed S
Exposed NS
Exposed NS
Exposed S
Exposed NS
Smoking status
Smoking status
CONCLUSIONS
REFERENCES
ACKNOWLEDGEMENTS
1) Mahata J., Basu A., Ghoshal S. et al., 2003.
Chromosomal aberrations and sister chromatid
exchanges in individuals exposed to arsenic
through drinking water in West Bengal, India.
Mutation Res. 534, 133-143. 2) Hei T.K., Filipic
M., 2004. Role of oxidative DNA damage in the
genotoxicity of arsenic. Free radical Biology
Medicine 37(5) 574-581. 3) Basu A., Mahata J.,
Roy A.K. et al., 2002. Enhanced frequency of
micronuclei in individuals exposed to arsenic
through drinking water in West Bengal, India.
Mutation Res. 516, 29-40. 4) Hartwig A., Asmuss
M., Ehleben I. et al., 2002. Interference by
toxic metal ions with DNA repair processes and
cell cycle control molecular mechanisms.Environm
ental Health Perspectives 110, 797-799. 5)
Rossman T.G., 2003. Mechanisms of arsenic
carcinogenesis an integrated approach. Mutation
Res. 533, 37-65.
We thank Sam Roesems and Gina Plas for their
expert technical assistance. This work was
supported by the Belgian Defence and by the EU
project Cytogenetic Biomarkers and Human Cancer
Risk (QLK4-2000-00628).

• Plant exposed workers (Group 1) may be at higher
  risk for increased genotoxic effects such as SCE,
  HFC, MN and CAs. Additional cytogenetic follow-up
  for the plant exposed workers is needed before
  drawing final conclusions.
• Continuous medical surveillance is needed for
  smokers exposed to arsenic compounds.