RESUMO
OBJECTIVE: To compare the applicability of two risk assessment methods for occupational health risk assessment in enterprises with 1-bromopropane(1-BP) production and utilization. METHODS: Three enterprises with 1-BP production and utilization were selected as the research subjects by a typical sampling method. The exposure concentration of time-weighted average of 1-BP-exposed in worker was detected. The non-carcinogenic health risk of 1-BP was assessed using the USA Environmental Protection Agency(EPA) inhalation risk(EPA assessment model) and the Ministry of Manpower of Singapore(MOM assessment model), and the results were compared. RESULTS: When the EPA method was used for the assessment, the risk assessment results of the four posts in the manufacturing enterprises were all negligible. In the enterprises that use 1-BP, the posts of cleaning machine B and clamping were of medium risk and the other four posts were of low risk based on the occupational exposure limit(OEL) in China used as the reference exposure concentration(RfC). When the 24-hour minimal risk level of USA Agency for Toxic Substances and Disease Registry was used as the RfC, the posts of cleaning machine B and clamping were of extreme high risk; the posts in cleaning machine A and checking were of high risk; the post in the cleaning machine D was of medium risk and the post of cleaning machine C was of low risk. When the MOM assessment model was used for evaluation, the four posts were of low risk in the 1-BP production enterprises. In the enterprises that use 1-BP, the posts of cleaning machine B and clamping were of high risk; the posts of cleaning machine A, cleaning machine D and checking were of medium risk; and the post of cleaning machine C was of low risk. CONCLUSION: When the OEL value is used for risk assessment, the MOM assessment method is more suitable than the EPA assessment method to assess occupational health risks of 1-BP.
RESUMO
<p><b>OBJECTIVE</b>To investigate acrylamide (ACR)-induced subacute neurotoxic effects on the central nervous system (CNS) at the synapse level in rats.</p><p><b>METHODS</b>Thirty-six Sprague Dawley (SD) rats were randomized into three groups, (1) a 30 mg/kg ACR-treated group, (2) a 50 mg/kg ACR-treated group, and (3) a normal saline (NS)-treated control group. Body weight and neurological changes were recorded each day. At the end of the test, cerebral cortex and cerebellum tissues were harvested and viewed using light and electron microscopy. Additionally, the expression of Synapsin I and P-Synapsin I in the cerebral cortex and cerebellum were investigated.</p><p><b>RESULTS</b>The 50 mg/kg ACR-treated rats showed a significant reduction in body weight compared with untreated individuals (P < 0.05). Rats exposed to ACR showed a significant increase in gait scores compared with the NS control group (P < 0.05). Histological examination indicated neuronal structural damage in the 50 mg/kg ACR treatment group. The active zone distance (AZD) and the nearest neighbor distance (NND) of synaptic vesicles in the cerebral cortex and cerebellum were increased in both the 30 mg/kg and 50 mg/kg ACR treatment groups. The ratio of the distribution of synaptic vesicles in the readily releasable pool (RRP) was decreased. Furthermore, the expression levels of Synapsin I and P-Synapsin I in the cerebral cortex and cerebellum were decreased in both the 30 mg/kg and 50 mg/kg ACR treatment groups.</p><p><b>CONCLUSION</b>Subacute ACR exposure contributes to neuropathy in the rat CNS. Functional damage of synaptic proteins and vesicles may be a mechanism of ACR neurotoxicity.</p>