DNA protein crosslinks (DPC) and mutation in the p53 tumour suppressor gene may be causally related and represent steps in the carcinogenicity of formaldehyde (FA). This has important implications for workers exposed to the latter.

Formaldehyde resins are used in producing adhesives for wood, plastics, textile, and leather while FA itself is a bactericide and tissue preservative. It is known to be a carcinogen; in vitro and in mammalian studies its primary genotoxic effect is the formation of DPC in target tissues but no studies on the latter had been conducted previously on humans.

The investigators examined DPC in peripheral blood mononuclear cells and p53 in serum from 186 workers in hospital laboratories (‘exposed’) and 213 hospital administrators (‘controls’).

DPC levels were significantly higher in the exposed group and the mean amount increased with increasing levels of exposure to FA, as determined by ambient air analysis. Additionally FA exposure increased the risk of having pantropic p53>150 pg/ml and mutant p53.

As FA undergoes exceptionally rapid biotransformation once absorbed there is no reliable direct biomarker. Thus, measuring DPC can be regarded as a surrogate for the dose of FA at critical target sites. The implications of this study are to provide a biologically plausible explanation for the epidemiological evidence of cancer risk from FA; and it may provide a method for screening exposed workers to identify those at higher risk.