IARC MONOGRAPHS ON THE EVALUATION OF CARCINOGENIC ...

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IARC MONOGRAPHS VOLUME 82
positive relationship was observed between styrene exposure and early colour vision
dysfunction in several of these studies, with effects detected at exposure concentrations
as low as 20 ppm [85 mg/m 3 ]. In one study, a dose–response relationship between the
concentration of mandelic acid in urine and colour vision loss was noted (Kishi et al.,
2001). Triebig et al. (2001) showed that styrene-induced colour vision dysfunction is
reversible when the person is in a styrene-free environment for four weeks.
In a study of mortality among styrene-exposed workers, an increased number of
deaths attributed to ‘symptoms, senility and ill-defined conditions’ was ascribed to a high
local registration of these conditions in comparison with national statistics (Bond et al.,
1992). Welp et al. (1996a) followed a cohort of workers in the reinforced-plastics
industry and found that mortality from diseases of the central nervous system, especially
epilepsy, increased with exposure to styrene. Exposure was evaluated as duration
(< 1–>10 years), average concentration (60–120 ppm [256–511 mg/m 3 ]) and cumulative
exposure (< 50–> 500 ppm–years [< 213–> 2130 mg/m 3 –years]). The effects of styrene
on the respiratory tract of workers exposed to concentrations above 100 mg/m 3 include
chronic bronchitis (Härkönen, 1977). Haematological changes (in blood coagulation and
fibrinolysis) have been observed (Chmielewski & Renke, 1976). Cases of styreneinduced
asthma (Moscato et al., 1987; Hayes et al., 1991) and one case of contact dermatitis
(Sjöborg et al., 1984) have also been reported. Welp et al. (1996b) reported that
mortality from pneumonia among more than 40 000 men and women in 660 European
factories manufacturing reinforced plastics appeared to be associated with exposure to
styrene, but mortality from bronchitis, emphysema and asthma was not. In a more recent
study, no relationship was observed between exposure to styrene and mortality from nonmalignant
respiratory diseases among 15 826 workers exposed to styrene (average
styrene concentrations were below 10 ppm [43 mg/m 3 ], with 14% of the workers exposed
to ≥ 60 ppm [256 mg/m 3 ]) in the reinforced-plastics and composites industry in the USA
(Wong & Trent, 1999).
Several studies have reported signs of liver damage, as measured by liver enzyme
activities in serum, but it was concluded in a review that no clear trend towards altered
liver function had been demonstrated (WHO, 1983). Elevated serum bile acid concentrations
were observed in one study (Edling & Tagesson, 1984) but not in another
(Härkönen et al., 1984).
More recently, two independent cross-sectional studies in 47 workers in the glass
fibre-reinforced plastics industry and in 21 boat and tank fabricators, both with separate
control groups, were carried out by Brodkin et al. (2001). Exposure to styrene was
assessed by measurements in blood and air samples. Workers were grouped as controls,
low-exposure (≤ 25.0 ppm [106 mg/m 3 ] styrene), or high-exposure (> 25.0 ppm styrene).
Direct bilirubin levels, a marker of altered hepatic clearance, increased with styrene
exposure. Hepatic transaminase activities (alanine and aspartate transaminases)
increased with styrene exposure when data from both studies were pooled.
Altered kidney function in styrene-exposed workers was measured by increased
urinary excretion of albumin (Askergren et al., 1981). Vyskocil et al. (1989) studied