28.02.2013 Views

Handbook of Solvents - George Wypych - ChemTech - Ventech!

Handbook of Solvents - George Wypych - ChemTech - Ventech!

Handbook of Solvents - George Wypych - ChemTech - Ventech!

SHOW MORE
SHOW LESS

You also want an ePaper? Increase the reach of your titles

YUMPU automatically turns print PDFs into web optimized ePapers that Google loves.

15.2.1 Use <strong>of</strong> breath monitoring 1091<br />

effect would be negligible the next morning. Breath samples collected the next morning<br />

would reflect exposure on preceding days and the measurements would be independent <strong>of</strong><br />

level <strong>of</strong> physical exertion. Finally, individual differences in body build and metabolism<br />

would have the greatest effect on breath levels, with the largest variations expected for metabolized<br />

solvents.<br />

Experimental data were used in a model, 59 which divided the body into four tissue<br />

compartments: vessel rich group, muscle group, fat group and liver. Metabolism was assumed<br />

to take place in the liver as a combination <strong>of</strong> a linear metabolic component and a Michaelis-Menten<br />

component. Metabolic parameters and partition coefficients determined for<br />

rats were scaled for body weight and were used in fitting results for humans. The model fit<br />

very well the data reported from other controlled human exposure studies. 51,52,54<br />

The BEI committee <strong>of</strong> the ACGIH recommends 2 three indices <strong>of</strong> PERC exposure:<br />

1) PERC in end-exhaled air collected prior to the shift after at least 2 consecutive<br />

workdays.<br />

2) PERC in blood collected prior to the shift after at least 2 consecutive workdays.<br />

3) Trichloroacetic acid (TCA) in urine voided at the end <strong>of</strong> the workweek. This index<br />

is recommended only as a screening test because <strong>of</strong> the variability associated with urinary<br />

excretion <strong>of</strong> TCA and, as such, no creatinine correction is necessary.<br />

15.2.1.7.2 Styrene<br />

The highest exposures to styrene take place in plants manufacturing glass-reinforced plastics,<br />

particularly during lamination, where there is considerable evaporation <strong>of</strong> styrene.<br />

Most <strong>of</strong> the inhaled styrene is absorbed and retained in the body. The first step in the major<br />

metabolic pathway is the formation <strong>of</strong> styrene-7,8-oxide (phenyloxirane), a reaction catalyzed<br />

by Cytochrome P-450 in the liver. The oxide is then hydrated to styrene glycol<br />

(1-phenyl-1,2-ethanediol) by microsomal epoxide hydratase. The styrene glycol is conjugated<br />

with beta-glucuronic acid, or is oxidized to mandelic acid and further to<br />

phenylglyoxylic acid. In humans, less than 5% <strong>of</strong> absorbed styrene is eliminated via the<br />

lung, whereas 90% is eliminated in the urine as mandelic and phenylglyoxylic acids.<br />

A number <strong>of</strong> chamber and field studies have been reported, where blood, exhaled air<br />

and urine have been studied as possible biological indicators. Although conditions and<br />

study design differed among studies, certain consistent patterns emerged, which formed the<br />

basis for subsequent recommendations.<br />

In an early series <strong>of</strong> chamber exposures, 60 nine healthy males were exposed to styrene<br />

concentrations <strong>of</strong> 50 to 370 ppm for periods ranging from 1 to 7 hours. Alveolar air samples<br />

were collected during and for 8 hours following exposure. The authors showed that the<br />

amounts <strong>of</strong> styrene present in the breath were directly related to the level and the duration <strong>of</strong><br />

exposure.<br />

In another study, 61 fourteen healthy males were exposed to 50 and 150 ppm <strong>of</strong> styrene<br />

in inspired air during rest and light (50 W) physical exercise. The duration <strong>of</strong> exposure for<br />

each styrene concentration was 30 minutes, with total pulmonary ventilation, cardiac output,<br />

and styrene concentration in alveolar air, arterial blood and venous blood measured<br />

during and after exposure. During exposure at rest to either 50 or 150 ppm, the alveolar air<br />

concentrations were about 20% <strong>of</strong> the inspired air concentrations. When alveolar ventilation<br />

almost tripled with exercise at 50 W, the alveolar air concentrations increased slightly,<br />

whereas arterial blood concentrations almost tripled. Alveolar air concentrations reached a<br />

plateau within a minute or so, that persisted throughout the 30-minute period. Arterial blood<br />

concentrations, however, rose rapidly during each such period and even more with increasing<br />

exercise intensity (50, 100 and 150 W). Venous blood concentrations also rose sharply<br />

during the 30-minute exposure periods without ever reaching a plateau. No linear relationship<br />

was found between exposure duration and arterial and venous blood concentrations,

Hooray! Your file is uploaded and ready to be published.

Saved successfully!

Ooh no, something went wrong!