Quality of Chemical Safety Information in Printing Industry.

OBJECTIVES: Employees in printing industries can be exposed to multiple solvents in their work environment. The objectives of this study were to investigate the critical components of chemical solvents by analyzing the components of the solvents and collecting the Safety data sheets (SDSs), and to evaluate the hazard communication implementation status in printing industries. METHOD: About 152 printing-related industries were recruited by area-stratified random sampling and included 23 plate-making, 102 printing and 27 printing-assistance companies in Taiwan. We analyzed company questionnaires (n = 152), SDSs (n = 180), and solvents (n = 20) collected from this sample of printing-related companies. RESULTS: Analytical results indicated that benzene and ethylbenzene, which were carcinogen and possibly carcinogen, were detectable in the cleaning solvents, and the detection rate were 54.5% (concentrations: <0.011-0.035 wt%) and 63.6% (concentrations: <0.011-6.22 wt%), respectively; however, neither compound was disclosed in the SDS for the solvents. Several other undisclosed components, including methanol, isopropanol and n-butanol, were also identified in the printing inks, fountain solutions and dilution solvents. We noted that, of the companies we surveyed, only 57.2% had a hazard communication program, 61.8% had SDSs on file and 59.9% provided employee safety and health training. We note that hazard communication programs were missing or ineffective in almost half of the 152 printing industries surveyed. CONCLUSIONS: Current safety information of solvents components in printing industries was inadequate, and many hazardous compounds were undisclosed in the SDSs of the solvents or the labels of the containers. The implementation of hazard communications in printing industries was still not enough for protecting the employees' safety and health.

CYP1A1 gene polymorphisms as a risk factor for pterygium.

PURPOSE: Both cytochrome P4501A1 (CYP1A1) and glutathione S-transferase M1 (GSTM1) have been demonstrated to be involved in the metabolism of polycyclic aromatic hydrocarbons (PAHs). BaP 7,8-diol 9,10-epoxide (BPDE), an ultimate metabolite of benzo(a)pyrene (BaP), attacks deoxyguanosine to form a BPDE-N2-dG adduct resulting in p53 gene mutations. Our previous report indicated that BPDE-like DNA adduct levels in pterygium were associated with CYP1A1 gene polymorphisms. Therefore, we hypothesize that the genetic polymorphisms of CYP1A1 and GSTM1 increase the risk for pterygium. METHODS: Two hundred-five pterygial specimens and 206 normal controls were collected in this study. For the analysis of CYP1A1 and GSTM1 gene polymorphisms, DNA samples were extracted from blood cells and then subjected to restriction fragment length polymorphism and polymerase chain reaction for the determination of mutation and genotype of CYP1A1 and GSTM1. RESULTS: There was a significant difference between the case and control groups in the CYP1A1 genotype (p=0.0161) but not in GSTM1 (p=1.000). The odds ratio of the CYP1A1 m1/m2 polymorphism was 1.327 (95% CI=0.906-2.079, p=0.135) and the m2/m2 polymorphism was 1.647 (95% CI=1.154-2.350, p=0.006), compared to the m1/m1 wild-type genotype. The GSTM1 polymorphisms did not have an increased odds ratio compared with the wild type. CONCLUSIONS: In conclusion, a CYP1A1 polymorphism is correlated with pterygium and might become a marker for the prediction of pterygium susceptibility.

E-cadherin promoter hypermethylation may contribute to protein inactivation in pterygia.

PURPOSE: Our recent reports indicated that the molecular changes of pterygia are similar to tumor cells. We believe that pterygia may have a similar mechanism in oncogenesis. Many studies have revealed that E-cadherin associated protein expression decreases in many tumors and pterygia. E-cadherin may be a marker for both tumor metastasis and prognosis. However, no studies have examined the reason for E-cadherin protein inactivation in pterygia. Therefore, this study aimed to analyze the association of E-cadherin promoter hypermethylation with protein inactivation in pterygial tissues. METHODS: E-cadherin methylation-status and the expression of E-cadherin and beta-catenin protein were studied using methylation-specific PCR and immunohistochemistry, respectively, on 120 pterygial specimens and 30 normal conjunctivas. RESULTS: Hypermethylation of E-cadherin gene promoter was detected in 32 (26.7%) of the 120 pterygial specimens. A total of 79 (65.8%) pterygial specimens tested positive for E-cadherin protein expression and 41 (34.2%) specimens tested negative. The E-cadherin staining was limited to the membrane of the epithelial layer. There was a reverse correlation between E-cadherin gene promoter hypermethylation and E-cadherin protein expression (p<0.0001). Aberrant localization of beta-catenin was higher in the E-cadherin negative group than in E-cadherin positive group. CONCLUSIONS: Our study demonstrates E-cadherin gene promoter hypermethylation were associated with low or absent expression of E-cadherin. Moreover, loss of E-cadherin protein may contribute to aberrant localization of beta-catenin. These data provide evidence that methylation exists in pterygia and may play a role in their development.