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Appendix D - Dossier (PDF) - Tera

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date: 20–JUL–2005<br />

5. Toxicity Substance ID: 71–43–2<br />

______________________________________________________________________________<br />

and external benzene exposures in this study. They also<br />

note<br />

that creatinine elimination increases with body mass, and<br />

that excretion of MA and HQ standardised per g creatinine<br />

approximates excretion standardised per kg body weight<br />

thereby providing a surrogate estimate of internal<br />

exposure.<br />

Based on this analysis, they suggest that children have a<br />

higher internal exposure than adults. The basis of this<br />

conclusion is not clear, however, given the probable<br />

contribution of dietary precursors to urinary MA and HQ.<br />

Source: A.K. Mallett Surrey<br />

Conclusion: Muconic acid and hydroquinone do not appear to be reliable,<br />

specific markers of low benzene exposure due to potential<br />

confounding by food–borne precursors of these substances.<br />

This may explain the absence of correlation between urinary<br />

metabolite levels and benzene exposure in this study.<br />

16–MAR–2004 (638)<br />

Type of experience: other: benzene oxide–albumin adducts in human blood<br />

Method: An expanded version of this study and its methods was<br />

reported subsequently by Qu et al. (2003) Validation and<br />

evaluation of biomarkers in workers exposed to benzene in<br />

China. Research Report 115, Health Effects Institute,<br />

Boston<br />

MA.<br />

<strong>Appendix</strong> D: Benzene SIDS <strong>Dossier</strong><br />

SUBJECTS AND METHODS<br />

Thirty benzene–exposed workers were recruited from three<br />

factories in Shanghai, China where benzene was used as a<br />

rubber solvent, in the manufacture of adhesive tape or in<br />

paint. Forty three control workers (frequency matched with<br />

exposed group by gender and age) were recruited from a<br />

sewing machine factory and an administrative facility in<br />

the<br />

same geographic region.<br />

EXPOSURE MESAUREMENTS<br />

Exposure to benzene was assessed measured by personal<br />

monitoring (passive; full work shift on 5 or 6 consecutive<br />

days).<br />

ADDUCT MEASUREMENTS<br />

Benzene oxide–albumin adducts (BO–Alb) in blood were<br />

determined by GC–MS in negative chemical ionisation mode.<br />

(Blood collection details not given).<br />

STATISTICAL METHODS<br />

Results of analyses for BO–Alb in blood and personal<br />

exposure data for the exposed worker population were<br />

natural<br />

log transformed and subject to regression analysis. This<br />

analysis was performed twice, once on the raw BO–Alb<br />

results<br />

and again after subtraction of the geometric mean value for<br />

the controls from data for the exposed population. Within<br />

– 765/957 –

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