The effect of cross-regional transport on ozone and particulate matter pollution in China: A review of methodology and current knowledge.

China is currently one of the countries impacted by severe atmospheric ozone (O3) and particulate matter (PM) pollution. Due to their moderately long lifetimes, O3 and PM can be transported over long distances, cross the boundaries of source regions and contribute to air pollution in other regions. The reported contributions of cross-regional transport (CRT) to O3 and fine PM (PM2.5) concentrations often exceed those of local emissions in the major regions of China, highlighting the important role of CRT in regional air pollution. Therefore, further improvement of air quality in China requires more joint efforts among regions to ensure a proper reduction in emissions while accounting for the influence of CRT. This review summarizes the methodologies employed to assess the influence of CRT on O3 and PM pollution as well as current knowledge of CRT influence in China. Quantifying CRT contributions in proportion to O3 and PM levels and studying detailed CRT processes of O3, PM and precursors can be both based on targeted observations and/or model simulations. Reported publications indicate that CRT contributes by 40-80 % to O3 and by 10-70 % to PM2.5 in various regions of China. These contributions exhibit notable spatiotemporal variations, with differences in meteorological conditions and/or emissions often serving as main drivers of such variations. Based on trajectory-based methods, transport pathways contributing to O3 and PM pollution in major regions of China have been revealed. Recent studies also highlighted the important role of horizontal transport in the middle/high atmospheric boundary layer or low free troposphere, of vertical exchange and mixing as well as of interactions between CRT, local meteorology and chemistry in the detailed CRT processes. Drawing on the current knowledge on the influence of CRT, this paper provides recommendations for future studies that aim at supporting ongoing air pollution mitigation strategies in China.

Regional PM2.5 pollution confined by atmospheric internal boundaries in the North China Plain: Analysis based on surface observations.

There are plenty of mesoscale meteorological discontinuities in the atmosphere, acting as atmospheric internal boundaries (AIBs). In conjunction with the atmospheric boundary layer in the vertical direction, they form confined three-dimensional structures that significantly affect air pollution. However, the role of AIBs in regional pollution has not been systematically elucidated. Based on surface observations, this study investigates PM2.5 pollution distributions under the forcing of various AIBs in the North China Plain. A total of 98 regional pollution episodes are identified during the autumn and winter of 2014-2020, and are further classified according to the impact of AIBs. In the pollution formation-maintenance stage, there are three categories. The frontal category (with a frequency of 41%), including the frontal trough type and frontal inverted trough type, displays the most polluted air masses along the mountains. The frontal AIB defines the lateral border of the pollution zone and forms a frontal inversion above, creating a closed and stable structure wherein the highest concentration of PM2.5 accumulates. The wind shear category (29%) is decided by the dynamic convergence AIB, which causes lighter PM2.5 pollution with diverse spatial patterns corresponding to west-southwest shear, southeast-east shear, and south-north shear. The topographic obstruction category (14%) presents as a narrow arc-shaped pollution belt at the foot of the windward mountains, resulting from the cold air damming AIB with dynamical obstruction and thermal stratification. Pollution diffuses in three ways: northwest, west, and northeast, respectively. The first one is the strongest and most frequent (42%), with both strong horizontal wind and vertical mixing. The second category is relatively rare (17%), characterized by foehn-induced active vertical ventilation. The last one is frequent (41%), but relatively weak, mainly relying on horizontal diffusion. Some evolution details of the AIB affecting PM2.5 pollution are also illustrated by a typical case.

Mechanism of haze pollution in summer and its difference with winter in the North China Plain.

Heavy haze pollution usually occurs in winter. However, according to the enhanced atmospheric boundary layer (ABL) field experiments conducted in the North China Plain (NCP) from 17 June to 6 July 2019, heavy haze pollution may also occur in summer, although with a lower probability. Winter haze pollution is significantly affected by adverse boundary layer meteorological conditions, whereas our study shows different mechanisms of summer haze pollution from that of winter. In summer, PM2.5 is distributed uniformly as a thick layer at a lighter pollution level; however, the PM2.5 column content in summer exceeds that in winter, suggesting that the better air quality in summer is mainly due to improved diffusion conditions. In summer, even under haze conditions, the ABL can develop over 1000 m and has a large ventilation similar to clean periods, which indicates both favourable vertical diffusion conditions and advection capability of the summer ABL. Unlike in winter, the heavy haze pollution in summer is often caused by regional transport which is related to local circulation. To explore the influence of different scale systems on summer haze pollution, we applied the spectral analysis method to surface PM2.5 concentrations. Strong periodicity of PM2.5 concentrations is found in 4-9 d and 1 d, corresponding to the impacts of large-scale synoptic system changes and the ABL evolution, respectively. The influence of weather change is much stronger than that of the ABL evolution on PM2.5 concentrations in summer. The resulting changes in PM2.5 concentrations are approximately 45 µg/m3 and 15 µg/m3, respectively. There has been a consensus on the importance of emission control in winter. And this study shows that heavy haze pollution can also occur in summer and regional joint emission control should also be emphasized in summer.

Facile Hydrothermal Synthesis of Chlorella-Derived Environmentally Friendly Fluorescent Carbon Dots for Differentiation of Living and Dead Chlorella.

The judgment of microalgae viability is a vital procedure in the process of microalgae culture and treatment, which also plays an important role in bioremediation, bioindication, and pharmacology fields. The current conventional methods for defining living/dead microalgal cells are complicated or laborious. Hence, developing a simple and reliable detection method for microalgae viability is still challenging. Here, we developed chlorella-based carbonized polymer dots (c-CPDs) by a hydrothermal method. Due to their small average size of 5.0 nm, obvious excitation-dependent emission, stable fluorescence properties, and low toxicity, c-CPDs could be used for distinguishing living or dead chlorella by testing different fluorescence characteristics of c-CPD-labeled chlorella. Compared with conventional cellular dyes used for differentiating living/dead microalgae, c-CPDs significantly reduced toxicity, showing good sensitivity and reliability. This work provided a method to prepare environmentally friendly carbon dots (CDs) using microalgae, which had potential to be prepared on a large scale and might be applied feasibly in the preparation of doped CDs by controlling the growth of chlorella.

[Association analysis of polymorphisms of metabolizing enzyme genes with chronic benzene poisoning based on logistic regression and multifactor dimensionality reduction].

OBJECTIVE: To explore the association of polymorphisms of metabolizing enzyme genes with chronic benzene poisoning (CBP) comprehensively by case-control design. METHODS: 152 CBP patients and 152 workers occupationally exposed to benzene without poisoning manifestations were investigated. 30 single nucleotide polymorphisms (SNPs) in 13 genes such as CYP2E1 were tested by PCR-RFLP, sequencing approaches. Logistic regression model was used to detect main effects and 2-order interaction effects of gene and/or environment. Multifactor dimensionality reduction (MDR) was used to detect high-order gene-gene or gene-environment interactions. RESULTS: Based on logistic regression, the main effects of GSTP1 rs947894, EPHX1 rs1051740, CYP1A1 rs4646903, CYP2D6 rs1065852 and rs1135840 were found to be significant (P < 0.05) while the confounding factors of sex, cigarette smoking, alcohol consumption and the intensity of benzene exposure were controlled. EPHX1 rs1051740 might be associated with CBP (P = 0.06). There existed 3 types of interactions were as followed: interactions of GSTP1 rs947894 with alcohol consumption, CYP2E1 rs3813867 with EPHX1 rs3738047, EPHX1 rs3738047 with alcohol consumption(P < 0.05), while the main effects of CYP2E1 rs3813867 and EPHX1 rs3738047 were not significant (P > 0.05). The other SNPs did not show any significant associations with CBP. According to MDR, a 3-order interaction with the strongest combined effect was found, i.e. the 3-factor combination of CYP1A1 rs4646903, CYP2D6 rs1065852 and CYP2D6 rs1135840. CONCLUSION: Gene-gene, gene-environment interactions are important mechanism to genetic susceptibility of CBP.

[Genetic polymorphism in XPD related to risks of chronic benzene poisoning].

OBJECTIVE: To explore the relation between genetic polymorphisms in XPD and risks of chronic benzene poisoning (CBP). METHODS: A case-control study was conducted. 152 CBP patients and 152 NCBP workers occupationally exposed to benzene were investigated. Polymerase chain reaction-restrained fragment length polymorphism technique (PCR-RFLP) was applied to detect the single nucleotide polymorphisms (SNPs) at c. 199, c. 201, c. 312 and c. 751 of XPD gene. RESULTS: No variant alleles was detected at c. 199 and c. 201 of XPD gene. In comparition with the individual genotypes of XPDc. 312Asp/Asp, the risk of CBP suffered from the individual genotype of XPDc. 312Asp/Asn + Asn/Asn decreased a 0.59 fold (ORadj = 0.59, 95% CI = 0.35-0.99, chi2 = 3.99, P < 0.05), when sex, workage and intensity of benzene exposure were adjusted. And in low intensity of benzene exposure group, the risk of CBP suffered from the individual genotypes of XPDc. 312Asp/Asn + Asn/Asn more decreased (ORadj = 0.13, 95% CI = 0.04-0.51, chi2 = 8.93, P < 0.01). CONCLUSION: Polymorphism of XPD Asp312Asn could contribute to altered risk of CBP.

Association of genetic polymorphisms in GADD45A, MDM2, and p14 ARF with the risk of chronic benzene poisoning in a Chinese occupational population.

Benzene reactive metabolites can lead to DNA damage and trigger the p53-dependent defense responses to maintain genomic stability. We hypothesized that the p53-dependent genes may play a role in the development of chronic benzene poisoning (CBP). In a case-control study of 303 patients with benzene poisoning and 295 workers occupationally exposed to benzene in south China, we investigated associations between the risk of CBP and polymorphisms in three p53-dependent genes. Potential interactions of these polymorphisms with lifestyle factors were also explored. We found p14(ARF) rs3731245 polymorphism was associated with risk of CBP (P=0.014). Compared with those carrying the GG genotype, individuals carrying p14(ARF) rs3731245 GA+AA genotypes had a reduced risk of CBP ([adjusted odds ratio (OR(adj))=0.57, 95%CI=0.36-0.89]. Further analysis showed p14(ARF) TGA/TAG diplotype was associated with an increased risk of CBP (P=0.0006), whereas p14(ARF) TGG/TAA diplotype was associated with a decreased risk of CBP (P=0.0000001). In addition, we found individuals carrying both MDM2 Del1518 WW genotype and p14(ARF) rs3731245 GA+AA genotypes had a lower risk of CBP (OR(adj)=0.25; 95%CI=0.10-0.62; P=0.003). Although these results require confirmation and extension, our findings suggest that genetic polymorphisms in p14(ARF) may have an impact on the risk of CBP in the study population.

Association of genetic polymorphisms, mRNA expression of p53 and p21 with chronic benzene poisoning in a chinese occupational population.

DNA damage induced by benzene reactive metabolites is thought of as an important mechanism underlying benzene hematotoxicity and genotoxicity, and genetic variation in cell-cycle control genes may contribute to susceptibility to chronic benzene poisoning (CBP). Using a case-control study that included 307 benzene-poisoned patients and 299 workers occupationally exposed to benzene in south China, we aimed to investigate the association between genetic polymorphisms of p53 and p21 and the odds of CBP. To investigate whether benzene exposure may influence mRNA expression of p53 and p21 in benzene-exposed workers, we also chose 39 CBP workers, 38 occupationally benzene-exposure workers, and 37 nonexposure workers in the same region of China. PCR-restriction fragment length polymorphism technique was applied to detect polymorphisms of p53 (rs17878362, rs1042522, and rs1625895) and p21 (rs1801270 and rs1059234), and real-time PCR was applied to detect the quantity of gene mRNA expression. We found that p21 C98A variant genotypes (CA+AA) or C70T variant genotypes (CT+TT) were associated with decreased odds of CBP [odds ratio (OR), 0.51; 95% confidence interval (95% CI), 0.32-0.83, and OR, 0.53; 95% CI, 0.29-0.95, respectively. Further analysis showed the decreased odds of CBP in the subjects with p21 CC/AT diplotype (OR, 0.51; 95% CI, 0.30-0.85). In addition, p53 mRNA expression of CBP workers or benzene-exposure workers was significantly lower than that of nonexposure workers. Although these results require confirmation and extension, our results show that polymorphisms in p21 may be protective against the risk of CBP in the Chinese occupational population.

Genetic polymorphisms in hMTH1, hOGG1 and hMYH and risk of chronic benzene poisoning in a Chinese occupational population.

Oxidative damage to DNA induced by benzene is an important mechanism of its genotoxicity, which leads to chronic benzene poisoning (CBP). Therefore, genetic variation in DNA repair genes may contribute to susceptibility to CBP in the exposed population. We hypothesized that single nucleotide polymorphisms (SNPs) in hMTH1, hOGG1 and hMYH genes are associated with risk of CBP. We genotyped SNPs at codon 83 of hMTH1, codon 326 of hOGG1, and codon 324 of hMYH in 152 CBP patients and 152 healthy workers occupationally exposed to benzene without poisoning manifestations. The genotypes were determined by polymerase chain reaction-restrained fragment length polymorphism (PCR-RFLP) technique. There were 2.51-fold [adjusted odds ratio (OR(adj)), 2.51; 95% CI, 1.14-5.49; P=0.02] and 2.49-fold (OR(adj), 2.49; 95% CI: 1.52-4.07; P<0.01) increased risk of CBP for individuals carrying genotypes of hMTH1 83Val/Met+Met/Met and hOGG1 326Cys/Cys, respectively. Compared with individuals carrying genotypes of hOGG1 326Cys/Cys and hMYH 324His/His at the same time, there was a 0.33-fold (OR(adj), 0.33; 95% CI: 0.15-0.72; P<0.05) decreased risk of CBP for those with genotypes of hOGG1 326Ser/Cys+Ser/Ser and hMYH 324His/Gln+Gln/Gln. In the smoking group, there was a 0.15-fold (OR(adj), 0.15; 95% CI, 0.03-0.68; P=0.01) decreased risk of CBP for subjects carrying genotypes of hMYH 324His/Gln+Gln/Gln compared with those of genotype of hMYH 324His/His. Therefore, our results suggested that polymorphisms at codons 83 of hMTH1 and codon 326 of hOGG1 might contribute to CBP in a Chinese occupational population.

[In vitro evaluation of cutaneous allergic reaction induced by chemicals using dendritic cells].

OBJECTIVE: To investigate the use of dendritic cells derived from mice bone marrow to evaluate the cutaneous allergic reaction induced by chemical sensitizers. METHODS: Dendritic cells derived from mice bone marrow were cultured and administrated with 2, 4-dinitrochlorobenzene (DNCB), nickel sulfate (NiSO4), sodium dodecyl sulfate (SDS) and hexyl cinnamic aldehyde (HCA), respectively. Cell membrane molecule CD86 and extracellular IL-1 beta, IL-6 and IL-12 were detected after 0, 1, 6, 12, 24, 36, 48 hour's administration, respectively. RESULTS: CD86 expression reached the highest level after exposure to DNCB for 48 h, and increased by about 279% compared with the control (P < 0.05), while it was lower than that of control after administrated with NiSO4 and HCA for 1 h and 6 h, and SDS for 36 h, respectively (P < 0.05). Extracellular IL-1 beta increased greatly after exposure to NiSO4 just for 1 h, with the maximum at 48 h (298 pg/ml, P < 0.05), and after exposure to HCA for 6 h, with maximum at 48 h (84 pg/ml, P < 0.05). However, it didn't fluctuate significantly after administrated with DNCB and SDS respectively, compared with the control. Extracellular IL-6 increased significantly after exposure to NiSO4 for 1 h, with the maximum at 24 h (2152 pg/ml, P < 0.05). After exposure to HCA, extracellular IL-6 reached the maximum at 1 h (1403 pg/ml), and then it was decreased quickly, but still higher than the control (P < 0.05), while it didn't change significantly after treatment with DNCB and SDS, compared with the control (P > 0.05). Extracellular IL-12 was not detected out among all the groups. CONCLUSION: Chemical sensitizer DNCB could induce the high expression of CD86 on DC membrane, and NiSO4 and HCA could induce DC to release IL-1 beta and IL-6. However, the irritant SDS had no such effect.

Polymorphisms in phase I and phase II metabolism genes and risk of chronic benzene poisoning in a Chinese occupational population.

It is widely accepted that the cytotoxicity and genotoxicity of benzene results from the action of reactive metabolites. Therefore, genetic variation in metabolic enzyme genes may contribute to susceptibility to chronic benzene poisoning (CBP) in the exposed population. Using a case-control study that included 268 benzene-poisoned patients and 268 workers occupationally exposed to benzene in South China, we aimed to investigate the association between single-nucleotide polymorphisms in genes with phase I and II of metabolism and risk of CBP. The TaqMan technique was used to detect polymorphisms of CYP1A1, CYP1A2, CYP1B1, ADH1B, EPHX1, EPHX2, NQO1, MPO, GSTP1 and UGT1A6 genes. We also explored potential interactions of these polymorphisms with lifestyle factors such as cigarette smoking and alcohol consumption. A weak positive association was found between glutathione S-transferase pi-1 (GSTP1) rs1695 polymorphism and the risk of CBP (P = 0.046), but this association was not statistically significant (P = 0.117) after adjustment for potential confounders. Further analysis showed that the risk of CBP increased in the subjects with EPHX1 GGAC/GAGT diplotype (P = 0.00057) or AGAC/GAGT diplotype (P = 0.00086). In addition, we found that alcohol drinkers with the EPHX1 rs3738047 GA + AA genotypes and non-alcohol drinkers with the GSTP1 rs1695 AA genotype tended to be more susceptible to benzene toxicity. Our results suggest that genetic polymorphisms in EPHX1 may contribute to risk of CBP in a Chinese occupational population.

[Intervention of nicotinamide on skin melanin genesis after UVA exposed].

OBJECTIVE: To investigate the interference effect of nicotinamide on UVA-induced melanin genesis and melanin transport in human skin melanocyte. METHODS: The optimum UVA dose expected to cause cell proliferation: 0.2 J/cm(2), nicotinamide was added immediately after the 0.2 J/cm(2) UVA exposure and the melanin content, cell cycles, cell apoptosis and mRNA express level were measured respectively. RESULTS: Melanin content in melanocytes was increased significantly after exposed to 0.2 J/cm(2) UVA. Melanin content in melanocytes was decreased after treatment with 10.0 mmol/ml nicotinamide following UVA exposure, but the cell cycles and the cell apoptosis rate were not significantly altered. mRNA express levels of TYR, TRP-1 were modulated by nicotinamide. CONCLUSION: Nicotinamide has more effect on decreasing melanin genesis after UVA exposure, nicotinamide also plays a role in modulating the mRNA express of TYR, TRP-1 gene. It is possible to consider nicotinamide as an efficient and safe sun screen to provide a certain level of protection for UVA exposed skin.

Genetic polymorphisms in CYP1A1, CYP2D6, UGT1A6, UGT1A7, and SULT1A1 genes and correlation with benzene exposure in a Chinese occupational population.

Metabolic enzymes involved in benzene activation or detoxification, including cytochrome P-450 1A1 (CYP1A1), cytochrome P-450 2D6 (CYP2D6), UDP-glucuronosyltransferase 1A6 (UGT1A6), UDP-glucuronosyltransferase1A7 (UGT1A7), and sulfotransferase 1A1 (SULT1A1), were studied for their roles in human susceptibility to benzene poisoning. All 304 subjects were investigated with a unitary questionnaire and their DNA was isolated from blood samples by a routine phenol-chloroform extraction. The study included 152 benzene poisoning patients, and 152 control workers occupationally exposed to benzene in South China. The genotypes were determined by polymerase chain reaction-restricted fragment length polymorphism (PCR-RFLP) technique with genomic DNA. No individuals had the CYP 2D6 c.212 G>A variant alleles in this study. There is no association between the UGT1A6 c.181 T>A, UGT1A7 c.208 Trp>Arg, and SULT1A1 c.638 G>A genotypes and increased risk of benzene-induced carcinogenesis. Although most of the CYP2D6 haplotypes did not show any significant difference, the CYP2D6 haplotype CYP2D6 c.188 C/C, C/T, and c.4268 C/C was significantly overrepresented in the case group (OR 4.02, 95% CI: 2.53-6.39) compared with in controls. Overall, our data suggested that individuals with CYP1A1 c.5639 T/T, CYP2D6 c.188 C/C, C/T, and CYP2D6 c.4268 C/C genotypes tend to be more susceptible to benzene toxicity.

[Relationship of genetic polymorphism in APE1 and ADPRT to risks of chronic benzene poisoning].

OBJECTIVE: To explore the relationship between genetic polymorphisms in apurinic/apyrimidinic endonuclease (APE1) and ADP ribosyltransferase (ADPRT) and individuals' susceptibility to chronic benzene poison ing (BP). METHODS: A case-control study was conducted. One hundred and fifty-two B P patients and 152 workers occupationally exposed to benzene without poisoning manifestations were investigated. The mismatched bases combined to create restriction site with restrained fragment length polymorphism technique (CRS-RFLP) was used for detecting the single nucleotide polymorphisms (SNPs) at Asp148Glu of APE1 gene and Val762Ala of ADPRT gene. RESULTS: There was no significant difference in the distribution of genotypes of APE1Asp148Glu and ADPRTVal762Ala between the patients and the control groups. Compared with individuals having genotype of APE1Asp148Glu T/T without habit of alcohol consumption, there was a 4.13 times increased risk of BP for the alcohol user with genotype of APE1Asp148Glu T/T (OR = 4.13, 95% CI: 1.07 - 15.85, P = 0.03). The analysis of Logistic regression showed that smoking may play some role in modifying the risk of cironic benzene poisoning (OR = 0.33, 95% CI: 0.14 - 0.75, P = 0.01). CONCLUSION: The genetic polymorphisms in APE1Asp148Glu, ADPRTVal762Ala are not related to the risk of BP. Potential interaction is found between alcohol consumption and polymorphism of APE1Asp148Glu. Further study is needed to elucidate this interaction.

[Genetic polymorphism of CYP-1A1, CYP2D6 and risks of chronic benzene poisoning].

OBJECTIVE: To explore the relationship between genetic polymorphisms of CYP-1A1 and CYP2D6 and risks of chronic benzene poisoning (BP). METHODS: A case control study was conducted. 152 BP patients and 152 workers occupationally exposed to benzene without poisoning manifestations were involved. Polymerase chain reaction followed by restriction fragment length polymorphism (PCR-RFLP) technology was used for detecting the single nucleotide polymorphisms (SNPs) of MspI in the non-coding region of CYP-1A1 gene and c.188, g.212 position in the first extron of CYP2D6 gene. RESULTS: The individuals with CYP1A1 MspI T/T genotype had a 1.32 times (95% CI: 1.05 approximately 1.65, P = 0.02) increased risk of BP compared with those carrying T/C and C/C genotypes. In no-smoking population, there was a 1.56 times (95% CI: 1.15 approximately 2.12, P = 0.003) increased risk of BP for subjects carrying CYP1A1 MspIT/T genotype compared with those carrying T/C and C/C genotypes. The individuals carrying CYP2D6 c.188 C/C or C/T genotype had a 1.23 times (95% CI: 1.05 approximately 1.42, P = 0.01) increased risk compared with those carrying T/T genotypes. In no-smoking population, there was a 1.23 times (95% CI: 1.04 approximately 1.47, P = 0.01) increased risk of BP for subjects carrying CYP2D6 c.188 C/C or C/T genotypes compared with those carrying T/T genotype. The single nucleotide polymorphism of g.212 position in the first extron of CYP2D6 gene had not been validated. CONCLUSION: The individuals with CYP2D6 c.188 C/C, CYP2D6 c.188 C/T and CYP1A1 MspIT/T genotypes tend to be more susceptible to benzene toxicity.

[Relationship between genetic polymorphism in hMTH1c.83, hOGG1c.326 and hMYHc.335 and risks of chronic benzene poisoning].

OBJECTIVE: To explore the relationship between genetic polymorphisms in hMTH1, hOGG1 and hMYH and risks of chronic benzene poisoning (CBP). METHODS: A case control study was conducted. One hundred and fifty-two BP patients and 152 workers occupationally exposed to benzene without poisoning manifestations were investigated. The polymerase chain reaction restrained fragment length polymorphism technique (PCR-RFLP) was applied to detect the single nucleotide polymorphisms (SNPs) on c.83 of hMTH1 gene, c.326 of hOGG1 gene and c.335 of hMYH gene. RESULTS: There were 2.51 times (OR(adj) = 2.51, 95% CI: 1.14-5.49, P = 0.02) and 2.49 times (OR(adj) = 2.49, 95% CI: 1.52-4.07, P < 0.01) risks of BP for individuals carrying genotypes of hMTH1c.83Val/Met + Met/Met or hOGG1c.326Cys/Cys compared with individuals carrying genotypes of hMTH1c.83Val/Val or hOGG1c.326Ser/Cys + Ser/Ser, respectively. Compared with individuals carrying genotypes of hOGG1c.326Cys/Cy and hMYHc.335 is/His at the same time, there was 0.33 times (OR(adj) = 0.33, 95% CI = 0.15-0.72, P = 0.01) risks of BP for these with genotypes of hOGG1c.326Ser/Cys + Ser/Ser and hMYHc.335His/Gln + Gln/Gln simultaneously. In the smoking group, there was 0.15 times (OR(adj) = 0.15, 95% CI: 0.03-0.68, P = 0.01) risks of BP for subjects carrying genotypes of hMYHc.335His/Gln + Gln/Gln compared with these carrying genotypes of hMYHc.335His/His. CONCLUSION: Polymorphisms of hMTH1 Val83 Met and hOGG1 Ser326Cys may contribute to altered risks of CBP, and potential interaction may exist among polymorphisms of hOGG1 Ser326Cys and hMYH His335Gln.

Genetic polymorphisms in XRCC1, APE1, ADPRT, XRCC2, and XRCC3 and risk of chronic benzene poisoning in a Chinese occupational population.

DNA damage induced by benzene is an important mechanism of its genotoxicity that leads to chronic benzene poisoning (CBP). Therefore, genetic variation in DNA repair genes may contribute to susceptibility to CBP in the exposed population. Because benzene-induced DNA damage includes single- and double-strand breaks, we hypothesized that single-nucleotide polymorphisms in X-ray repair cross-complementing group 1 (XRCC1), apurinic/apyrimidinic endonuclease (APE1), ADP ribosyltransferase (ADPRT), X-ray repair cross-complementing group 2 (XRCC2), and X-ray repair cross-complementing group 3 (XRCC3) are associated with risk of CBP. We genotyped single-nucleotide polymorphisms at codons 194, 280, and 399 of XRCC1, codon 148 of APE1, codon 762 of ADPRT, codon 188 of XRCC2, and codon 241 of XRCC3 in 152 CBP patients and 152 healthy workers frequency matched on age and sex among those who were occupationally exposed to benzene. The genotypes were determined by PCR-RFLP technique with genomic DNA. We found that no individuals had the XRCC2 codon 188 variant alleles or Met/Met genotype of XRCC3 codon 241 in this study population. However, individuals carrying the XRCC1 194Trp allele (i.e., Arg/Trp+Trp/Trp genotypes) had a decreased risk of CBP [adjusted odds ratio (OR(adj)), 0.60; 95% confidence interval (95% CI), 0.37-0.98; P = 0.041] compared with subjects with the Arg/Arg genotype whereas individuals carrying the XRCC1 280His allele (i.e., Arg/His+His/His genotypes) had an increased risk of CBP compared with those with the Arg/Arg genotype (OR(adj), 1.91; 95% CI, 1.17-3.10; P = 0.009). The analysis of haplotypes of polymorphisms in XRCC1 showed that there was a 2.96-fold (OR, 2.96; 95% CI, 1.60-5.49; chi(2) = 12.39, P = 0.001) increased risk of CBP for subjects with alleles of XRCC1 194Arg, XRCC1 280His, and XRCC1 399Arg compared with those carrying alleles of XRCC1 194Arg, XRCC1 280Arg, and XRCC1 399Arg. Therefore, our results suggest that polymorphisms at codons 194 and 280 of XRCC1 may contribute to CBP in a Chinese occupational population.

[The intervention of nicotinamide on skin melanocyte's cell proliferation after UVA (365 nm) exposed.].

OBJECTIVE: To investigate the interference effect of nicotinamide on UVA-induced cell proliferation in human skin melanocyte. METHODS: To apply the optimum UVA dose expected to cause cell proliferation: 0.2 cm2, nicotinamide was added after the 0.2 cm2 UVA exposure immediately or 48 h later, then the rate of cell proliferation, calcium concentration and the activities of Na+-K+, Ca2+-ATP enzymes of melanocytes were measured respectively. RESULTS: After treatment with 1.000 mg/ml nicotinamide following UVA exposure, the rate of cell proliferation was decreased significantly 24 hours later. Treatment with 0.125 mg/ml nicotinamide 48 hours after UVA exposure also significantly inhibited the cell proliferation; 1.25 mg/ml nicotinamide increased calcium concentration in cells; 0.250 mg/ml nicotinamide increased the activities of Na+-K+, Ca2+-ATP enzymes in melanocytes (P < 0.05). CONCLUSION: Nicotinamide has more obvious effect on inhibiting melanocyte's proliferation if added immediately following UVA exposure. Our discovery indicated that nicotinamide may affect the melanocyte through modulating the calcium concentration. It is possible to consider nicotinamide as an efficient and safe sun screen to provide a certain level of protection for UVA exposed skin.