Neurotoxicity effect of formaldehyde on occupational exposure and influence of individual susceptibility to some metabolism parameters.

Over the years, neurotoxicity and cognitive dysfunction have separately been associated with endogenous formaldehyde and reduction of acetylcholine signals. However, a limited number of studies have shown a relationship between cholinergic neurotransmitter and formaldehyde exposure. Therefore, the aim of this study was to assess the neurological effect on workers from melamine-dish preparation workshop, who were exposed to formaldehyde. A total of 35 formaldehyde-exposed workers were compared with 32 control employees from the food industry. Occupational exposure to formaldehyde was conducted using the National Institute of Occupational Safety and Health 3500 methods. Using the Ellman method, acetylcholinesterase (AChE) as a biomarker for neurotoxicity was analyzed in blood erythrocyte. The effects of alcohol dehydrogenase III (ADH3) and Mn-superoxide dismutase (Mn-SOD) polymorphism were used to survey the level of AChE activity. In this study, it was found that exposure to airborne formaldehyde increased from 0.024 to 0.74 ppm and the median personnel exposure was 0.057. Induction of AChE activity was observed in formaldehyde-exposed workers as compared with the control group (p < 0.01), while AChE activity increased in 64 % of the exposed subjects. Spearman's correlation (p < 0.02) was used to evaluate the association between AChE activity and occupational exposure to formaldehyde. Exposed subjects containing ADH32-2 genotype had higher AChE than others. The findings of this study suggest that the neurotoxic effect of formaldehyde depends on the AChE activity, which is affected by metabolism. It can be concluded that cholinergic signal reduction in cases of cognitive dysfunction could be associated with endogenous formaldehyde.