Occupational health risk assessment of workplace solvents and noise in the electronics industry using three comprehensive risk assessment models.

Background: Occupational hazards such as solvents and noise in the electronics industry are serious. Although various occupational health risk assessment models have been applied in the electronics industry, they have only been used to assess the risks of individual job positions. Few existing studies have focused on the total risk level of critical risk factors in enterprises. Methods: Ten electronics enterprises were selected for this study. Information, air samples and physical factor measurements were collected from the selected enterprises through on-site investigation, and then the data were collated and samples were tested according to the requirements of Chinese standards. The Occupational Health Risk Classification and Assessment Model (referred to as the Classification Model), the Occupational Health Risk Grading and Assessment Model (referred to as the Grading Model), and the Occupational Disease Hazard Evaluation Model were used to assess the risks of the enterprises. The correlations and differences between the three models were analyzed, and the results of the models were validated by the average risk level of all of the hazard factors. Results: Hazards with concentrations exceeding the Chinese occupational exposure limits (OELs) were methylene chloride, 1,2-dichloroethane, and noise. The exposure time of workers ranged from 1 to 11 h per day and the frequency of exposure ranged from 5 to 6 times per week. The risk ratios (RRs) of the Classification Model, the Grading Model and the Occupational Disease Hazard Evaluation Model were 0.70 ± 0.10, 0.34 ± 0.13, and 0.65 ± 0.21, respectively. The RRs for the three risk assessment models were statistically different (P < 0.001), and there were no correlations between them (P > 0.05). The average risk level of all of the hazard factors was 0.38 ± 0.18, which did not differ from the RRs of the Grading Model (P > 0.05). Conclusions: The hazards of organic solvents and noise in the electronics industry are not negligible. The Grading Model offers a good reflection of the actual risk level of the electronics industry and has strong practicability.

Application of multiple occupational health risk assessment models in the prediction of occupational health risks of n-Hexane in the air-conditioned closed workshop.

Background: n-Hexane (NH) poisoning is a common occupational poisoning in the hardware and electronics industries. However, there is few research data on risk assessment of positions using NH in enclosed workshops. It is very important to assess the risk level of these positions and put forward effective measures and suggestions. Methods: The information of selected companies and air samples were collected through on-site investigation, and data collation and sample testing were carried out according to the requirements of Chinese standards. The Control of Substances Hazardous to Health (COSHH) Essential, the EPA non-carcinogenic risk assessment model, the Singapore exposure index method and the Chinese semi-quantitative risk assessment models were used to assess the risks of NH. Results: The working hours of the exposure groups, printing groups and packing groups all exceeded 9 h per day, less than 30% of each similar exposure groups (SEG) was equipped with the local exhaust ventilation, and 11.1% of the cleaning group and 8.3% of the printing group had NH concentrations in the air that exceeded the Chinese occupational exposure limit (OEL). In the EPA non-carcinogenic risk assessment model, each SEG was evaluated at high risk. In the Chinese semi-quantitative risk assessment models, all of the work groups of exposure groups, 91.7% of the work groups of printing groups, 77.8% of the work groups of printing groups, and 57.1% of the work groups of printing groups were evaluated at unacceptable risk. More than 40.0% of the work groups of printing groups and cleaning groups and over 20.0% of the work groups of exposure groups and packing groups were evaluated at high risk in the Chinese semi-quantitative risk assessment models. Conclusions: The Chinese exposure index method and the synthesis index method may have a stronger practicability. Some work groups that use NH in air-conditioned enclosed workshops in China, especially the cleaning groups, are still in a high-risk state. It is necessary to increase protective measures and strengthen occupational hygiene management to reduce risks.

Targeted proteomic scan identifies alteration of serum proteins among workers occupationally exposed to low levels of trichloroethylene.

Occupational exposure to trichloroethylene (TCE) has been associated with alterations in B-cell activation factors and an increased risk of non-Hodgkin's lymphoma (NHL). Here, we aimed to examine the biological processes influenced by TCE exposure to understand the underlying molecular mechanisms. This cross-sectional molecular epidemiology study included data of 1317 targeted proteins in the serum from 42 TCE exposed and 34 unexposed factory workers in Guangdong, China. We used multivariable linear regressions to identify proteins associated with TCE exposure and examined their exposure-response relationship across categories of TCE exposure (unexposed, low exposed: <10 ppm, high exposed: ≥10 ppm). We further examined pathway enrichment of TCE-related proteins to understand their biological response. Occupational exposure to TCE was associated with lower levels of tumor necrosis factor receptor superfamily member 17 (TNFRSF17; ß = -.08; p-value = .0003) and kynureninase (KYNU; ß = -.10, p-value = .002). These proteins also showed a significant exposure-response relation across the unexposed, low exposed, and high exposed workers (all p-trends < .001, false discovery rate [FDR] < 0.20). Pathway analysis of TCE-related proteins showed significant enrichment (FDR < 0.05) for several inflammatory and immune pathways. TCE exposure was associated with TNFRSF17, a key B-cell maturation antigen that mediates B-cell survival and KYNU, an enzyme that plays a role in T-cell mediated immune response. Given that altered immunity is an established risk factor for NHL, our findings support the biological plausibility of linking TCE exposure with NHL.

Occupational trichloroethylene exposure and antinuclear antibodies: a cross-sectional study in China.

OBJECTIVES: There has been concern over the possible risk of autoimmune diseases from exposure to trichloroethylene (TCE), an industrial solvent and common pollutant near hazardous waste sites. Studies of TCE-exposed lupus-prone mouse strains have reported increases in serum antinuclear antibodies (ANAs), a marker of autoimmunity, and autoimmune pathologic changes, while epidemiologic studies have provided limited support for an association between TCE exposure and scleroderma. To investigate exposure-related biologic evidence of autoimmunity in humans, we measured ANA levels in sera from a cross-sectional study of TCE-exposed (n=80) and TCE-unexposed (n=96) workers in Guangdong, China. METHODS: Full-shift personal air exposure measurements for TCE were taken prior to blood collection. Serum ANAs were detected by immunofluorescence on HEp-2 cells. We calculated ORs and 95% CI relating levels of TCE exposure (categorised using tertiles as cut-points) and ANA positivity (1+ intensity at 1:320 dilution) using multivariable logistic regression. RESULTS: Samples from 16 of 176 participants were ANA-positive. We found higher levels of TCE exposure (concentrations>17.27 ppm) to be associated with an elevated odds of ANA positivity (OR 4.7, 95% CI 1.3 to 16.8) compared with unexposed controls. This association remained after excluding two subjects with diagnosed autoimmune disease (OR 4.5, 95% CI 1.2 to 16.2). We did not observe an association with ANAs at lower exposure levels. CONCLUSIONS: Our findings, to our knowledge the first direct human evidence of an association between TCE exposure and systemic autoimmunity, provide biologic plausibility to epidemiologic evidence relating TCE and autoimmune disease.

Self-administration of complex decongestive therapy facilitated by the mobile application WeChat improves lymphedema and quality of life in breast cancer survivors: an observational study.

Background: Lymphedema is the most common complication of breast cancer patients. Complex decongestive therapy (CDT) is often recommended but the efficacy varies due to the complexity of management. This study investigated a novel model of CDT based on a mobile application with the aim of improving the management of lymphedema in China. Methods: We developed a novel model of CDT for breast cancer survivors with lymphedema, including 5 days of CDT therapy with training provided by medical staff in the outpatient clinic and 3 weeks of self-administrated CDT with daily online instructions during phase I, and a life-long maintenance treatment with online instructions once a week for phase II, which delivered by WeChat public accounts. The breast cancer and lymphedema symptom experience index (BCLE-SEI) and the Short-Form Health Survey (SF-36) were used to assess lymphatic symptoms and quality of life. Arm volume and lymphatic symptoms were assessed at baseline, and at 5 days, 1 month, and 3 months post-treatment. The quality of life was assessed at baseline and at 3 months post-treatment. Results: A total of 88 patients with lymphedema were recruited, of whom, 61 followed the protocols and were further analyzed for this study. The mean relative excess arm volume (EAV) was reduced from a baseline value of 30.72% to 22.05%, 18.46%, and 16.67% at 5 days, 1 month, and 3 months post-therapy, respectively (P=0.000). The BCLE-SEI scores of lymphatic pain, heaviness, and impaired limb mobility were all significantly improved after 3 months of treatment (P<0.05). Moreover, according to the subscale of SF-36, the general health and vitality were significantly improved after 3 months of therapy (56.64 vs. 62.93, P=0.008; and 64.26 vs. 70.08, P=0.024, respectively). Conclusions: The proposed model of CDT based on the mobile application WeChat achieved promising outcomes. The volume of the affected arm, the lymphedema symptoms, and the quality of life were all significantly improved.

Epigenetic aging biomarkers and occupational exposure to benzene, trichloroethylene and formaldehyde.

Epigenetic aging biomarkers are associated with increased morbidity and mortality. We evaluated if occupational exposure to three established chemical carcinogens is associated with acceleration of epigenetic aging. We studied workers in China occupationally exposed to benzene, trichloroethylene (TCE) or formaldehyde by measuring personal air exposures prior to blood collection. Unexposed controls matched by age and sex were selected from nearby factories. We measured leukocyte DNA methylation (DNAm) in peripheral white blood cells using the Infinium HumanMethylation450 BeadChip to calculate five epigenetic aging clocks and DNAmTL, a biomarker associated with leukocyte telomere length and cell replication. We tested associations between exposure intensity and epigenetic age acceleration (EAA), defined as the residuals of regressing the DNAm aging biomarker on chronological age, matching factors and potential confounders. Median differences in EAA between exposure groups were tested using a permutation test with exact p-values. Epigenetic clocks were strongly correlated with age (Spearman r > 0.8) in all three occupational studies. There was a positive exposure-response relationship between benzene and the Skin-Blood Clock EAA biomarker: median EAA was -0.91 years in controls (n = 44), 0.78 years in workers exposed to <10 ppm (n = 41; mean benzene = 1.35 ppm; p = 0.034 vs. controls), and 2.10 years in workers exposed to ≥10 ppm (n = 9; mean benzene = 27.3 ppm; p = 0.019 vs. controls; ptrend = 0.0021). In the TCE study, control workers had a median Skin-Blood Clock EAA of -0.54 years (n = 71) compared to 1.63 years among workers exposed to <10 ppm of TCE (n = 27; mean TCE = 4.22 ppm; p = 0.035). We observed no evidence of EAA associations with formaldehyde exposure (39 controls, 31 exposed). Occupational benzene and TCE exposure were associated with increased epigenetic age acceleration measured by the Skin-Blood Clock. For TCE, there was some evidence of epigenetic age acceleration for lower exposures compared to controls. Our results suggest that some chemical carcinogens may accelerate epigenetic aging.

The prediction of occupational health risks of benzene in the printing industry through multiple occupational health risk assessment models.

Background: Benzene poisoning is a common occupational poisoning event in the printing industries. Up to now there is still a lack of research data on risk assessment of benzene operations in enclosed workshops. It is crucial to assess the risk level of these positions and put forward effective measures and suggestions. Methods: The information of selected companies and air samples were collected through on-site investigation, data collation and sample testing were carried out according to the requirements of Chinese standards. The Control of Substances Hazardous to Health (COSHH) Essential, the EPA non-carcinogenic risk assessment model, the Singapore exposure index method and the Chinese semi-quantitative risk assessment models were used to assess the risks of benzene. Results: The exposed groups all worked more than 8 h per day, and the cleaning, pasting, and packaging groups used general ventilation rather than local ventilation. 28.6% of the printing group and 16.7% of the pasting group had benzene concentrations that exceeded the permissible concentration-time weighted average (PC-TWA) in China. Over 60.0% of the work groups were evaluated at high risk and over 20% of the work groups were evaluated at high cancer risk by the risk assessment models. Conclusion: The Chinese exposure index method and the synthesis index method may have a stronger practicability. The printing and pasting groups may have a higher risk for benzene exposure. It is necessary to increase protective measures and strengthen occupational hygiene management to reduce risks.

Aberrant expression of SNHG12 contributes to N, N-dimethylformamide-induced hepatic apoptosis both in short-term and long-term DMF exposure.

N, N-Dimethylformamide (DMF) can cause liver damage in occupationally exposed workers, but the molecular mechanism of DMF-induced liver damage has not been fully elucidated. Researches have proved that lncRNA plays a major function in chemical-induced liver toxicity and can be used as a biomarker and therapeutic target for liver injury. In order to verify that lncRNA also participates in DMF-induced liver damage, we treated HL-7702 cells with 75 or 150 mM DMF, and obtained lncRNA expression profiles through high-throughput sequencing. Among the differentially expressed lncRNAs, lncRNA SNHG12 was proved to be significantly downregulated in DMF-treated HL-7702 cells and participate in DMF-mediated apoptosis, even under long-term low-dose DMF exposure (5-10 mM, 8 weeks). In addition, according to bioinformatics analysis, miR-218-5p is expected to be a potential target of SNHG12, which was verified by the dual luciferase reporter assay in HEK293FT cells. MiR-218-5p mimic can induce apoptosis in HL-7702 cells. Among the predicted targets of miR-218-5p, protein kinase C epsilon (PRKCE) was reported to be involved in apoptosis, and was indeed downregulated by miR-218-5p mimic in our study. Further experiments showed that changes of the expression of SNHG12 can affect the expression of PRKCE. In the epidemiological study of occupational population, we also found that SNHG12 was downregulated in the serum exosomes of workers exposed to DMF. These results indicated that SNHG12 can mediate DMF-induced apoptosis of HL-7702 cells through miR-218-5p/PRKCE pathway.

Human exposure to trichloroethylene is associated with increased variability of blood DNA methylation that is enriched in genes and pathways related to autoimmune disease and cancer.

Human exposure to trichloroethylene (TCE) is linked to kidney cancer, autoimmune diseases, and probably non-Hodgkin lymphoma. Additionally, TCE exposed mice and cell cultures show altered DNA methylation. To evaluate associations between TCE exposure and DNA methylation in humans, we conducted an epigenome-wide association study (EWAS) in TCE exposed workers using the HumanMethylation450 BeadChip. Across individual CpG probes, genomic regions, and globally (i.e., the 450K methylome), we investigated differences in mean DNA methylation and differences in variability of DNA methylation between 73 control (< 0.005 ppm TCE), 30 lower exposed (< 10 ppm TCE), and 37 higher exposed ( ≥ 10 ppm TCE) subjects' white blood cells. We found that TCE exposure increased methylation variation globally (Kruskal-Wallis p-value = 3.75e-3) and in 25 CpG sites at a genome-wide significance level (Bonferroni p-value < 0.05). We identified a 609 basepair region in the TRIM68 gene promoter that exhibited hypomethylation with increased exposure to TCE (FWER = 1.20e-2). Also, genes that matched to differentially variable CpGs were enriched in the 'focal adhesion' biological pathway (p-value = 2.80e-2). All in all, human exposure to TCE was associated with epigenetic alterations in genes involved in cell-matrix adhesions and interferon subtype expression, which are important in the development of autoimmune diseases; and in genes related to cancer development. These results suggest that DNA methylation may play a role in the pathogenesis of TCE exposure-related diseases and that TCE exposure may contribute to epigenetic drift.

Association between occupational exposure to trichloroethylene and serum levels of microRNAs: a cross-sectional molecular epidemiology study in China.

OBJECTIVES: The objective of our study was to evaluate the association between occupational exposure to trichloroethylene (TCE), a suspected lymphomagen, and serum levels of miRNAs in a cross-sectional molecular epidemiology study of TCE-exposed workers and comparable unexposed controls in China. METHODS: Serum levels of 40 miRNAs were compared in 74 workers exposed to TCE (median: 12 ppm) and 90 unexposed control workers. Linear regression models were used to test for differences in serum miRNA levels between exposed and unexposed workers and to evaluate exposure-response relationships across TCE exposure categories using a three-level ordinal variable [i.e., unexposed, < 12 ppm, the median value among workers exposed to TCE) and ≥ 12 ppm)]. Models were adjusted for sex, age, current smoking, current alcohol use, and recent infection. RESULTS: Seven miRNAs showed significant differences between exposed and unexposed workers at FDR (false discovery rate) < 0.20. miR-150-5p and let-7b-5p also showed significant inverse exposure-response associations with TCE exposure (Ptrend= 0.002 and 0.03, respectively). The % differences in serum levels of miR-150-5p relative to unexposed controls were - 13% and - 20% among workers exposed to < 12 ppm and ≥ 12 ppm TCE, respectively. CONCLUSIONS: miR-150-5p is involved in B cell receptor pathways and let-7b-5p plays a role in the innate immune response processes that are potentially important in the etiology of non-Hodgkin lymphoma (NHL). Further studies are needed to replicate these findings and to directly test the association between serum levels of these miRNAs and risk of NHL in prospective studies.

Alterations in immune and renal biomarkers among workers occupationally exposed to low levels of trichloroethylene below current regulatory standards.

OBJECTIVES: The occupational exposure limit for trichloroethylene (TCE) in different countries varies from 1 to 100 ppm as an 8-hour time-weighted average (TWA). Many countries currently use 10 ppm as the regulatory standard for occupational exposures, but the biological effects in humans at this level of exposure remain unclear. The objective of our study was to evaluate alterations in immune and renal biomarkers among workers occupationally exposed to low levels of TCE below current regulatory standards. METHODS: We conducted a cross-sectional molecular epidemiology study of 80 healthy workers exposed to a wide range of TCE (ie, 0.4-229 ppm) and 96 comparable unexposed controls in China, and previously reported that TCE exposure was associated with multiple candidate biological markers related to immune function and kidney toxicity. Here, we conducted further analyses of all of the 31 biomarkers that we have measured to determine the magnitude and statistical significance of changes in the subgroup of workers (n=35) exposed to <10 ppm TCE compared with controls. RESULTS: Six immune biomarkers (ie, CD4+ effector memory T cells, sCD27, sCD30, interleukin-10, IgG and IgM) were significantly decreased (% difference ranged from -16.0% to -72.1%) and one kidney toxicity marker (kidney injury molecule-1, KIM-1) was significantly increased (% difference: +52.5%) among workers exposed to <10 ppm compared with the control group. These associations remained noteworthy after taking into account multiple comparisons using the false discovery rate (ie, <0.20). CONCLUSION: Our results suggest that occupational exposure to TCE below 10 ppm as an 8-hour TWA may alter levels of key markers of immune function and kidney toxicity.

Evidence for Adaptive Response in a Molecular Epidemiological Study of the Inhabitants of a High Background-radiation Area of Yangjiang, China.

Our previous studies have shown that cancer mortality in high background-radiation areas of China was lower than that in a control area, indicating the possibility of an adaptive response in high background-radiation areas. Our aim is to determine the effect of low-dose radiation on the level of DNA oxidative damage, DNA damage repair, antioxidant capacity, and apoptosis in high background-radiation area and control area populations of Guangdong through a molecular epidemiological study in order to identify adaptive response. Blood samples were collected from male residents aged 50 to 59 y in a high background-radiation area (Yangjiang) and a control area (Enping), and activities of superoxide dismutase, glutathione, catalase, total antioxidant capacity, and expression of O6-methylguanine-DNA methyltransferase gene (MGMT), human 8-oxoguanine DNA N-glycosylase 1 gene (hOGG1), proapoptotic genes and antiapoptotic genes, oxidative-stress-related genes, as well as concentrations of 8-OHdG, TrxR, HSP27, and MT-COX2 were determined. The activities of antioxidative enzymes, relative mRNA expression level of DNA repair genes, antiapoptotic genes, oxidative-stress-related genes HSPB1 and MT-COX2, and the concentration of antioxidant index TrxR in the high background-radiation area population increased significantly compared to the control population (p < 0.05). The relative mRNA expression level of proapoptotic genes and the concentration of DNA oxidative damage index 8-OHdG were significantly lower in the high background-radiation area compared to those in the control area (p < 0.05). In conclusion, under long-term, natural, high background, ionizing radiation, DNA damage-repair capacity and antioxidant capacity of inhabitants in the high background-radiation area may be enhanced. Additionally, it could induce up regulation of cell-survival gene expression and down regulation of apoptotic gene expression. It might be speculated that enhanced antioxidant and DNA repair capacity and inhibition of apoptosis might play important roles in adaptive response of low-dose radiation in high background-radiation areas.

Cooking Coal Use and All-Cause and Cause-Specific Mortality in a Prospective Cohort Study of Women in Shanghai, China.

BACKGROUND: Nearly 4.3 million deaths worldwide were attributable to exposure to household air pollution in 2012. However, household coal use remains widespread. OBJECTIVES: We investigated the association of cooking coal and all-cause and cause-specific mortality in a prospective cohort of primarily never-smoking women in Shanghai, China. METHODS: A cohort of 74,941 women were followed from 1996 through 2009 with annual linkage to the Shanghai vital statistics database. Cause-specific mortality was identified through 2009. Use of household coal for cooking was assessed through a residential history questionnaire. Cox proportional hazards models estimated the risk of mortality associated with household coal use. RESULTS: In this cohort, 63% of the women ever used coal (n = 46,287). Compared with never coal use, ever use of coal was associated with mortality from all causes [hazard ratio (HR) = 1.12; 95% confidence interval (CI): 1.05, 1.21], cancer (HR = 1.14; 95% CI: 1.03, 1.27), and ischemic heart disease (overall HR = 1.61; 95% CI: 1.14, 2.27; HR for myocardial infarction specifically = 1.80; 95% CI: 1.16, 2.79). The risk of cardiovascular mortality increased with increasing duration of coal use, compared with the risk in never users. The association between coal use and ischemic heart disease mortality diminished with increasing years since cessation of coal use. CONCLUSIONS: Evidence from this study suggests that past use of coal among women in Shanghai is associated with excess all-cause mortality, and from cardiovascular diseases in particular. The decreasing association with cardiovascular mortality as the time since last use of coal increased emphasizes the importance of reducing use of household coal where use is still widespread. CITATION: Kim C, Seow WJ, Shu XO, Bassig BA, Rothman N, Chen BE, Xiang YB, Hosgood HD III, Ji BT, Hu W, Wen C, Chow WH, Cai Q, Yang G, Gao YT, Zheng W, Lan Q. 2016. Cooking coal use and all-cause and cause-specific mortality in a prospective cohort study of women in Shanghai, China. Environ Health Perspect 124:1384-1389; http://dx.doi.org/10.1289/EHP236.

Circulating immune/inflammation markers in Chinese workers occupationally exposed to formaldehyde.

BACKGROUND: Formaldehyde has been classified as a human myeloid leukemogen. However, the mechanistic basis for this association is still debated. OBJECTIVES: We aimed to evaluate whether circulating immune/inflammation markers were altered in workers occupationally exposed to formaldehyde. METHODS: Using a multiplexed bead-based assay, we measured serum levels of 38 immune/inflammation markers in a cross-sectional study of 43 formaldehyde-exposed and 51 unexposed factory workers in Guangdong, China. Linear regression models adjusting for potential confounders were used to compare marker levels in exposed and unexposed workers. RESULTS: We found significantly lower circulating levels of two markers among exposed factory workers compared with unexposed controls that remained significant after adjusting for potential confounders and multiple comparisons using a false discovery rate of 10%, including chemokine (C-X-C motif) ligand 11 (36.2 pg/ml in exposed versus 48.4 pg/ml in controls, P = 0.0008) and thymus and activation regulated chemokine (52.7 pg/ml in exposed versus 75.0 pg/ml in controls, P = 0.0028), suggesting immunosuppression among formaldehyde-exposed workers. CONCLUSIONS: Our findings are consistent with recently emerging understanding that immunosuppression might be associated with myeloid diseases. These findings, if replicated in a larger study, may provide insights into the mechanisms by which formaldehyde promotes leukemogenesis.

Bisphenol A stimulates human lung cancer cell migration via upregulation of matrix metalloproteinases by GPER/EGFR/ERK1/2 signal pathway.

Lung cancer is one of the leading causes of cancer deaths worldwide. Recent evidences indicated that bisphenol A (BPA), a wide contaminant with endocrine disrupting activity, could enhance the susceptibility of carcinogenesis. Although there are increasing opportunities for lung cells exposure to BPA via inhalation, there is no study concerning the effects of BPA on the development of lung cancer. The present study revealed that BPA less than 10(-4)M had limited effects on the proliferation of lung cancer A549 cells, however, BPA treatment significantly stimulated the in vitro migration and invasion of cells combing with the morphological changes and up regulation of matrix metalloproteinase-2 (MMP-2) and MMP-9. G-protein-coupled estrogen receptor (GPER), while not estrogen receptor α/ß (ERα/ß), mediated the BPA induced up regulation of MMPs. Further, BPA treatment induced rapid activation of ERK1/2 via GPER/EGFR. GPER/ERFR/ERK1/2 mediated the BPA induced upregulation of MMPs and in vitro migration of lung cancer A549 cells. In summary, our data presented here revealed for the first time that BPA can promote the in vitro migration and invasion of lung cancer cells via upregulation of MMPs and GPER/EGFR/ERK1/2 signals, which mediated these effects. This study suggested that more attention should be paid on the BPA and other possible environmental estrogens induced development of lung cancer.

Household air pollution and lung cancer in China: a review of studies in Xuanwei.

Over half of the world's population is exposed to household air pollution from the burning of solid fuels at home. Household air pollution from solid fuel use is a leading risk factor for global disease and remains a major public health problem, especially in low- and mid-income countries. This is a particularly serious problem in China, where many people in rural areas still use coal for household heating and cooking. This review focuses on several decades of research carried out in Xuanwei County, Yunnan Province, where household coal use is a major source of household air pollution and where studies have linked household air pollution exposure to high rates of lung cancer. We conducted a series of case-control and cohort studies in Xuanwei to characterize the lung cancer risk in this population and the factors associated with it. We found lung cancer risk to vary substantially between different coal types, with a higher risk associated with smoky (i.e., bituminous) coal use compared to smokeless (i.e., anthracite) coal use. The installation of a chimney in homes resulted in a substantial reduction in lung cancer incidence and mortality. Overall, our research underscores the need among existing coal users to improve ventilation, use the least toxic fuel, and eventually move toward the use of cleaner fuels, such as gas and electricity.