Cell signaling regulates cell proliferation, survival, and migration, and abnormal kinase activity is often implicated in cancer. Although kinases are key targets for anticancer therapy, drug-induced compensatory signaling and pathway rewiring often drive acquired resistance. These compensatory responses enable tumor cells to maintain proliferation and survival, contributing to acquired drug resistance. In this study, we investigated adaptive responses following the knockout of four specific kinase genes, ERK2, PLK1, PIK3CA, and PAK4, using HCT-116, a human colorectal cancer cell line. Using CRISPR-Cas9, we generated individual knockout cell lines and conducted quantitative proteomic and phosphoproteomic profiling using isobaric tagging and tandem mass tag (TMTs) to evaluate alterations in the signaling landscape. Our integrated analysis quantified 7,531 proteins and 10,877 phosphopeptides, revealing kinase-specific patterns of compensatory signaling. ERK2 knockout was associated with activation of MAPK- and PI3K/AKT-related kinases, whereas PIK3CA knockout induced extensive proteomic remodeling and engagement of pro-survival phosphorylation programs, illustrating distinct modes of signaling network rewiring. Integration of kinase-substrate enrichment analysis (KSEA) with global proteomic data revealed that adaptive kinase activity was largely uncoupled from protein abundance and uncovered a synthetic lethal interaction between ERK2 loss and RPS6KB1 inhibition. Collectively, these findings elucidate how targeted kinase loss drives homeostatic signaling networks in cancer cells. By systemically characterizing cellular-level signaling changes and contextualizing them within known kinase pathways, our results provide insights into synthetic lethality and identify potential therapeutic targets to counteract adaptive resistance to kinase inhibitors.

Antibody-drug conjugates (ADCs) require antibodies with both high specificity and efficient internalization, features often overlooked by conventional discovery pipelines that rely on preselected antigens and recombinant proteins. Here, we describe an integrated phenotypic platform that combines target-unbiased live-cell biopanning with in situ chemical cross-linking and mass spectrometry to concurrently identify internalizing antibodies and their membrane-bound cognate antigens in a native cellular context. Using this approach, we identified 2E7, an antibody with rapid internalization and specificity for the integrin α3β1 (ITGA3B1) heterodimer. Integrated transcriptomic and proteomic analyses revealed pronounced overexpression of ITGA3B1 across multiple solid tumors, with particularly elevated levels in aggressive bladder cancer subtypes. A 2E7-MMAE (monomethyl auristatin E) ADC exhibited potent, dose-dependent antitumor activity in bladder cancer xenograft models, leading to tumor regression and prolonging survival. This study establishes a generalizable framework for function-first ADC discovery and nominates ITGA3B1 as a promising therapeutic target in bladder cancer.

Operational radioactive waste from routine 18F and 13N production was characterized at eight medical cyclotron facilities. The samples comprised 79 spent anion-exchange cartridges and 50 liquid-waste samples, including recovery and rinse water. Gamma-emitting radionuclides were quantified by HPGe spectrometry using geometry-matched certified reference materials prepared from actual QMA and SAX cartridges and a matching liquid-sample container. Tritium was measured by liquid scintillation counting in 18 cartridges and 47 liquid samples. Gamma activities were corrected to the end of bombardment and normalized to production yield where appropriate. Thirteen gamma-emitting activation radionuclides were identified originating predominantly from the Havar foil. Significant inter-facility differences remained for 11 of 12 radionuclides evaluated among facilities with matched cyclotron and target specifications. Associations with proton beam energy and integrated charge were radionuclide dependent. Waste-stream distributions reflected physicochemical behavior, with 51Cr, 95mTc, 181W and 183Re preferentially retained by QMA cartridges and 76–78% of 56Co, 57Co and 58Co transferred to recovery water. Tritium retention by QMA cartridges was negligible. Median tritium activities were 1.6×108 Bq L-1 in recovery water, 9.4×106 Bq L-1 in post-synthesis rinse water and 4.9×105 Bq L-1 in pre-synthesis rinse water. All spent cartridges exceeded the clearance level at EOB but were predicted to satisfy it after approximately 2.5–11.1 years of decay storage. Gamma-emitting radionuclides in the liquid streams could be managed through decay storage or removal, whereas tritium remained the controlling radionuclide for discharge. These findings provide a measurement-based framework for managing solid and liquid waste from medical cyclotron facilities.

Background: Radiotherapy eliminates most tumor cells but spares persister tumor cells that evade cell death and drive relapse. Increasing evidence suggests that stromal components of the tumor microenvironment influence treatment responses, yet whether macrophages actively reprogram tumor-intrinsic stress responses to promote radioresistance remains unclear. Here, we investigated the mechanisms by which macrophage–tumor cell interactions regulate ferroptosis and tumor survival after irradiation. Methods: We used macrophage–tumor cell coculture systems, Transwell separation assays, and 3D microfluidic models to examine contact-dependent effects on tumor survival following irradiation. Kinome-wide small interfering RNA screening, RNA sequencing, lipidomic profiling, and quantitative proteomic analysis of secretomes were performed to identify signaling pathways and metabolic changes. Genetic and pharmacological perturbation of Ephrin receptor b4 (Ephb4) signaling were evaluated in vitro and in syngeneic mouse tumor models. Clinical relevance was assessed using transcriptomic analyses and immunohistochemical staining of patient tumor specimens. Results: Macrophage contact reduced lipid peroxidation and cell death in irradiated tumor cells in a contact-dependent manner. Kinome screening identified Ephb4 as a key mediator induced by irradiation in tumor cells. Ephb4 engagement with ephrinb2 on macrophages initiated bidirectional signaling that increased expression of ferroptosis-protective genes (solute carrier family 7 member 11 [ Slc7a11 ], solute carrier family 3 member 2 [ Slc3a2 ], and glutathione peroxidase 4 [ Gpx4 ]) in tumor cells while activating the toll-like receptor 2- nuclear factor-kappa B pathway and interleukin-6 (IL-6) production in macrophages. Macrophage-derived IL-6 further sustained ferroptosis resistance in tumor cells, and Ephb4-driven secretion of cathepsin S amplified macrophage IL-6 production through a feedforward loop. Genetic or pharmacological inhibition of Ephb4 restored lipid peroxidation and markedly enhanced radiosensitivity in vitro and in vivo. Analysis of patient datasets demonstrated increased EPHB4 expression following radiotherapy and an association between high EPHB4 expression, reduced ferroptosis signatures, and poor treatment response. Conclusions: These findings identify a macrophage-driven ferroptosis evasion program that enables tumor cell survival after irradiation and demonstrate that Ephb4 coordinates bidirectional tumor–macrophage signaling to sustain this resistance. Targeting the Ephb4–ephrinb2 axis represents a potential strategy to enhance ferroptosis and improve radiotherapy efficacy in resistant tumors.

Kidneys are highly susceptible to metabolic changes associated with diabetes, which contribute to the progression of chronic kidney disease (CKD). Among the various cell types in the kidney, proximal tubular epithelial cells (PTECs) are particularly affected by diabetes. However, accurate detection and quantification of essential energy coenzymes such as nicotinamide adenine dinucleotide hydrogen (NADH) and flavin adenine dinucleotide (FAD) in PTECs have been challenging. In this study, we employed fluorescence lifetime imaging (FLIM) with a phasor analysis approach to quantitatively assess metabolic activity specific to PTECs in diabetic kidneys. We analyzed NADH and FAD lifetime in PTEC cells through FLIM analysis and also analyzed metabolic changes in human kidney tissue according to the CKD stage. Furthermore, we compared metabolic changes following glucagon-like peptide-1 receptor agonist (GLP-1RA) treatment using db/db mice. Our results demonstrated a significant reduction in NADH lifetime in both the mitochondria and cytoplasm of PTECs under high glucose conditions. Phasor analysis in db/db mice revealed shortened NADH and FAD lifetimes, which were quantitatively validated by increased NADH and decreased FAD production in db/db kidneys, indicating a high redox ratio in diabetic kidneys. Additionally, the phasor plot and lifetime measurements effectively reflected metabolic alterations in db/db kidneys in response to GLP-1RA treatment. In the kidneys of patients with type 2 diabetes, the peak region of the phasor plot shifted counterclockwise toward longer lifetimes as CKD progressed compared to normal kidneys. Quantitative imaging using FLIM in diabetic kidneys enables the detection and measurement of NADH and FAD with spatial information in PTECs, thereby providing insights into the progression of diabetic kidney disease and the response to treatment.

Emergency workers responding to nuclear power plant accidents may be exposed to high radiation dose rates. Therefore, when deploying emergency workers, it is necessary to estimate dose distribution within the work area and establish work plans based on this information. This study optimized a Kriging interpolation-based dose distribution estimation algorithm to address limitations in handling extreme values, reflecting spatial trends, optimizing parameters, and improving computational efficiency. Five methodological improvements were implemented: drift-based estimation for coordinate-dependent trends, the robust Cressie-Hawkins estimator, Weighted Least Squares (WLS) fitting for theoretical variogram derivation, Restricted Maximum Likelihood (REML) for parameter optimization, and the Moving Window technique for computational efficiency. The optimized algorithm was validated against Monte Carlo N-Particle (MCNP) code results for Waste Evaporator Room, Holdup Tank Room and Waste Drum Leakage scenarios. Compared to the conventional algorithm, the developed algorithm achieved average error reductions of 82%, 85% and 97% in the respective scenarios, with computational time reduced by approximately 80%. Even using only 10% of measurement points, error rates remained below 17%, demonstrating effective dose distribution estimation with limited measured values. These results are expected to contribute to dose map generation during nuclear emergencies and worker exposure management according to the ALARA principle.

Abstract Early detection of Alzheimer’s disease (AD) is critical for preventing disease progression. Blood platelets have emerged as a useful peripheral source for AD diagnosis. However, the identification of proteomics-based platelet biomarkers of mild cognitive impairment (MCI) and AD in relation to amyloid β (Aβ) deposition remains largely unexplored. In this study, we compared four groups from 18 participants: subjective memory impairment (SMI, n = 4) as cognitive normal controls, MCI without Aβ deposition (MCI-A(+), n = 5), MCI with Aβ deposition (MCI-A(−), n = 5), and AD (n = 4). We conducted in-depth platelet protein profiling using high-throughput LC–MS/MS with tandem mass tag labeling. Among the total 4,524 proteins detected, we identified both unique and overlapping differentially expressed proteins in MCI-A(+), MCI-A(−), and AD compared with SMI. Hierarchical clustering analysis revealed seven distinct patterns of proteomic alterations across groups. Functional network and gene ontology enrichment analyses indicated that each cluster was associated with specific processes, including platelet activation, AD, and apoptotic signaling pathways. Notably, upregulated proteins in MCI-A(−) and AD were linked to endomembrane system organization. Furthermore, we quantified the relative abundance of multiple protein candidates that were significantly altered in MCI-A(−) and AD compared with SMI and MCI-A(+). Our findings highlight several platelet proteins–ATP6V0C, AP4B1, RAB2B, PSMD9, FKBP1B, and mTOR–as potential molecular targets for predicting AD at the stage of MCI with Aβ deposition, providing new insights into amyloid-related neurodegeneration.

Metabolic shifts are crucial for cellular proliferation, however, the roles of various metabolic pathways and their interconnections in NSCLC remain unclear. This lack of understanding in metabolic shifts precludes better cancer management as well as effective therapeutic interventions. To bridge this gap, using network biology and RNA expression data complemented with wet lab experiments, metabolism in NSCLC has been studied in detailed furnishing new insights and therapeutic avenues. This study has revealed that the Malate-Aspartate Shuttle (MAS) is the backbone of nitrogen metabolic circuit, i.e., pyrimidine and arginine metabolic pathways. Several genes from the MAS (GOT1, GOT2, MDH2) are differentially regulated and are the target of therapeutic interventions, further providing the relevance of this network. Furthermore, when GOT1 was downregulated, it affected the expression of several cell cycle related genes (CCNA2, CCNB1, CCND1) and VEGF in KRAS mutated cell lines suggesting potential synthetic lethality interaction. Therefore, these experiments provide concrete evidence that MAS components, particularly GOT1, is a potential therapeutic candidate in NSCLC that could further evaluated in broader experimental conditions.

In patients with type 2 diabetes mellitus (T2DM) inadequately controlled with metformin and sulfonylurea, evidence directly comparing glucagon-like peptide-1 receptor agonists and sodium–glucose cotransporter 2 inhibitors as add-on therapy is limited; therefore, we compared dulaglutide and empagliflozin in this setting. This 12-week, single-center, randomized, open-label, parallel-group pilot study included a 24-week observational extension. Patients with HbA1c≥7.0% receiving stable doses of metformin and glimepiride were randomized to dulaglutide 0.75 mg/week or empagliflozin 10 mg/day. Doses were uptitrated at week 4 if tolerated and maintained for 12 weeks, with follow-up until week 36. The primary endpoint was the change in HbA1c at week 12. Secondary endpoints included changes in glycemic and obesity-related parameters. Exploratory analyses were performed to assess plasma metabolite profiles using liquid chromatography-mass spectrometry, and gut microbiota using 16S rRNA gene sequencing. Twenty-four patients completed the 12-week study (dulaglutide, n=13; empagliflozin, n=11). Both treatments significantly reduced HbA1c at week 12, with no significant between-group difference. Empagliflozin significantly reduced HOMA-IR, whereas dulaglutide significantly increased HOMA-β. At week 12, empagliflozin was associated with greater reductions in body weight and body fat compared with dulaglutide, whereas these differences were attenuated at week 36. Exploratory analyses suggested potential, modest treatment-related differences in plasma metabolite profiles and microbiome–metabolic associations, without marked alterations in overall microbial diversity. As add-on therapy to metformin and sulfonylurea, both dulaglutide and empagliflozin improved glycemic control, with no significant between-group difference observed in this exploratory pilot study. Empagliflozin induced earlier weight loss, whereas dulaglutide showed more gradual weight reduction over time, accompanied by exploratory findings suggesting possible differences in plasma and microbiome-related metabolic signatures.

Immune status critically affects cancer progression and therapy responses. This study aimed to identify plasma proteome changes in immunosuppressive cancer and potential biomarkers predicting systemic immunosuppression. Mouse models of syngeneic breast tumors (benign 67NR and malignant 4T1) were used to collect plasma samples. Plasma samples from naive mice and both early- and late-stage tumor-bearing mice were subjected to liquid chromatography-mass spectrometry (LC-MS) analysis. 4T1-bearing mice showed systemic immunosuppression characterized by significant generation of myeloid-derived suppressor cells (MDSCs) as early as 7 days after tumor implantation, unlike 67NR tumors. LC-MS identified 1086 proteins across the five experimental groups, with 27 proteins showing group-specific expression in 4T1 blood compared with 67NR blood. Immune-related proteins osteopontin, lactotransferrin, calreticulin, and peroxiredoxin 2 were selected as potential biomarkers of MDSC-producing breast cancer. These markers were expressed in cancer cells or MDSC in the 4T1 model, and osteopontin and peroxiredoxin 2 were associated with low survival probability and high recurrence in patients with triple-negative breast cancer. Our findings suggest that MDSC-producing immunosuppressive cancers have unique plasma proteomes, offering additional insights into cancer immune status.

HRAS is often overactivated in breast cancer, whereas mutations are rare in this malignancy. This study was aimed to determine how overexpressed wild-type HRAS (HRASWT) plays an oncogenic role in human breast cancer progression. The activated form of non-mutagemic HRASWT is highly overexpressed in aggressive triple-negative breast cancer (TNBC) compared with less invasive luminal breast tumor as well as normal mammary tissues. A qPCR assay showed that TNBC cells selectively overexpress HRASWT. Notably, HRAS directly interacted with and stabilized NRF2 whereas KRAS barely bound to NRF2. Further, HRASWT exerted its oncogenic capability by inducing interaction between NRF2 and STAT3. Such interaction was observed in TNBC tissues, but not other subtypes of breast cancer. Combined silencing of NRF2 and STAT3 suppressed TNBC growth to a greater extent than that achieved with single knockdown of individual genes. RNA sequencing analysis revealed expression profiles for genes related to cell migration which may account for synergistic oncogenic activity of NRF2 and STAT3. Our results suggest that NRF2 is a potential effector of HRAS that regulates downstream signaling in a KEAP1-independent manner. Non-mutated HRAS overexpression, in cooperation with NRF2, promotes the progression of breast carcinoma and might represent a novel therapeutic target against TNBC.

Background: In order to gain approval of decommissioning of nuclear power plants (NPPs), the operator has to submit a final decommissioning plan (FDP) to the regulatory body. The safety assessment is an essential part to be described in the FDP. In safety assessment, dose of the general public near the plant site due to decommissioning activities should be evaluated and described. As gaseous radioactive effluents are expected to be released in the process of decommissioning, it is necessary to assess the public dose. In this study, we assessed the public dose due to gaseous radioactive effluents released in NPP decommissioning activities.Materials and Methods: The source term of gaseous radioactive effluent was set based on the decommissioning scenarios suggested in the NUREG-0130. The critical group assumed the maximum individual for adults on the exclusion area boundary. Public exposure pathway was set in accordance with the guideline 2.2 of the Korea Institute of Nuclear Safety (KINS). In addition, the public dose was assessed through the GASPAR computer code with the factors suggested by the KINS.Results and Discussion: In the decommissioning scenario, the source term for gaseous radioactive effluent was set by using the nuclide fraction according to the contamination type of structures, systems, components in the reference reactor. As a result of the public dose assessment,total annual public dose in the overall decommissioning scenario was 1.95×10–2 μSv/yr. Segmentation on non-activated stainless steel task was the highest at 1.43×10–2 μSv/yr. In the overall scenario, the nuclide with the highest contribution to the public dose was Co-60. As a result of the assessment, it was found that the public dose due to the gaseous radioactive effluent during the decommissioning of the NPP was insignificant compared to the legal dose limit.Conclusion: The results of this study can be used as a basis for radiological safety assessment and the management of radioactive effluents in the decommissioning of NPP.

In water treatment facilities, naturally occurring radionuclides of soil and rock may be accumulated in groundwater during the treatment of drinking water. The objective of this study is to assess internal radiation doses due to NORM inhalation by workers in water treatment facilities in Korea. We analyzed flow of groundwater in water treatment facilities. Airborne particle concentration and activity concentration were measured using a large-capacity, individual air sampler and HPGe detector. The annual internal radiation dose ranged from 9.52 × 10–7 to 3.42 × 10–5 mSv y−1, which was less than the annual dose limit of the general public of 1 mSv y−1.

Diabetic retinopathy (DR) is a leading cause of blindness in adults under 40 in the developed world, with a significant proportion progressing to vision-threatening stages such as proliferative diabetic retinopathy (PDR) and neovascular glaucoma (NVG). This study aims to explore the molecular mechanisms underlying the progression from nonproliferative DR to PDR and NVG, focusing on identifying potential biomarkers and therapeutic targets. Utilizing discovery-based proteomics, specifically label-free quantification and tandem mass tag, we analyzed aqueous humor (AH) proteins obtained during cataract surgery or anterior chamber paracentesis from patients with nonproliferative DR, PDR, and NVG. Validation of marker candidates for each disease state was conducted using triple quadrupole-MS for targeted protein quantification. Our proteomic analysis identified 2255 proteins, and gene ontology analysis and functional annotation highlighted key biological processes implicated in DR, such as lens development, immune responses, and lipid metabolism. Validation of potential biomarkers identified 20 proteins with significant concentration changes, including several candidates with diagnostic utility based on ROC curve analysis. Further investigation into clinical relevance revealed that crystallin gamma-S is strongly associated with cataract severity, highlighting its role as a potential marker for ocular complications in DR. Importantly, we identified that the pathological factors driving DR progression have a much greater impact than age, a previously known variable, in shaping the proteomic landscape of AH. Additionally, proteins associated with macular degeneration (CA1, CA2, and HBA1) were uncovered, providing new insights into overlapping mechanisms between DR and other retinal diseases. Finally, proteins linked to panretinal photocoagulation treatment, including APOB and CST6, were identified, suggesting their involvement in the therapeutic response and post-treatment adaptation. These findings underscore the potential of AH proteomics in uncovering predictive biomarkers and elucidating the molecular pathogenesis of DR and its complications.

In Korea, coal-fired power plants manage fly ash by landfilling, which can cause radiological impacts on the general public. Therefore, a radiation dose assessment must be performed to verify the radiological safety of the general public around the coal-fired power plant. The objective of this study is to assess the radiation dose to the general public in Korean coal-fired power plants. To achieve this, we investigated the radioactivity concentration of fly ash generated from coal-fired power plants. The exposure scenarios were established based on the purpose of the site utilization and characteristics of the general public. The RESRAD-OFFSITE was used to assess the radiation dose. The radiation dose ranged from 2.36 × 10-5 ~ 5.60 × 10-2 mSv yr-1, which was lower than the annual dose limit regulated by the Nuclear Safety Act. The results of this study can be used as technical data for the radiological safety management of a Korean naturally occurring radioactive material facility.

As research into cancer biology progresses, multiomics analyses have become essential for unraveling its molecular complexities. However, sample availability remains a challenge due to factors such as collection procedures and long-term storage effects. Archived samples present an opportunity to expand multiomics studies, but concerns persist regarding storage duration's impact on data reliability. This study examines the genomic, transcriptomic, and proteomic profiles of samples stored for over a decade. Transcriptomic analysis revealed a decline in read counts for protein-coding genes but preserved core gene expression patterns. Proteomic measurements remained stable, with minimal changes in post-translational modifications. While phosphorylation and acetylation rates were largely unaffected, a slight increase in modification frequencies was observed. Housekeeping genes and proteins exhibited consistent expression across samples, yet proteomic differences between the tumor and normal tissues were distinct. Despite technical variations in transcriptomic data, essential transcription factors and kinases retained functionality. These findings underscore the viability of archived samples for multiomics research, enabling broader investigations into cancer biology and providing insights into molecular mechanisms. By leveraging archived specimens, researchers can overcome sample limitations and advance precision oncology efforts, ultimately deepening our understanding of cancer at the systems level.

Background: Beryllium-7 (Be-7), influenced by various environmental factors, is valuable for tracking radioactive material migration due to its short half-life and dynamic atmospheric distribution. These properties make Be-7 particularly useful for assessing the behavior of radioactive substances under changing environmental conditions or after radiation incidents. This study aims to establish foundational data by examining the correlation between Be-7 concentrations and environmental factors specific to the Republic of Korea. Materials and Methods: Be-7 radiation concentrations from 2013 to 2022 were collected from the National Environmental Radiation Survey Report of the Korea Institute of Nuclear Safety. Precipitation, humidity, particulate matter (PM10), and atmospheric pressure data were sourced from the Korea Meteorological Administration and the Ministry of Environment. Monthly and seasonal trends were analyzed, and Pearson correlation coefficients were used to assess the relationship between Be-7 concentrations and environmental factors, with the significance evaluated usingp-values. Results and Discussion: Analysis showed consistent nationwide trends, with Be-7 concentrations significantly decreasing each summer. Precipitation and humidity peaked in summer and negatively correlated with Be-7 concentrations, whereas PM10 and atmospheric pressure were lowest in summer and positively correlated with Be-7 concentrations. All correlations hadp-values below 0.001, indicating statistical significance. Conclusion: The findings indicate a significant relationship between Be-7 concentrations and environmental factors in the Republic of Korea, offering essential data for future research on radioactive material migration and informing environmental radiation safety strategies.

General radiography has the highest usage among diagnostic radiology in Korea, resulting in high radiation dose by general radiography. For the medical radiation safety of patients, it is necessary to evaluate Korean population dose by general radiography. In this study, collective dose and per capita effective dose from general radiography in the Korean population were calculated. To this end, the raw data on the usage of general radiography in Korea as of 2017 was analyzed. Moreover, information on radiation dose from domestic general radiography was collected and PCXMC was used to evaluate the effective dose for patients during general radiography. As of 2017, the usage rate for lower extremity and chest examinations was high, accounting for more than 20 % of the total general radiography examinations. The effective dose depending on the examination type was the highest for whole-spine AP (1.06 mSv), followed by whole-spine LAT (0.61 mSv), and lumbar spine AP (0.51 mSv). As a result of evaluating Korean population dose by general radiography, the collective dose was 22,066 man center dot Sv and the per capita effective dose was 0.43 mSv. The evaluation results of the Korea population dose obtained from this study can contribute to patient dose management in general radiography.

Water treatment facilities are facilities that use groundwater to produce potable water. Groundwater can contain radon which is a naturally occurring radionuclide, and water treatment facility workers who directly handle groundwater are at risk of internal exposure from radon inhalation. The objective of this study is to assess the internal radiation dose from radon inhalation in water treatment facility workers in Korea. To achieve this, we analyzed work processes in 6 water treatment facilities in Korea, and main process areas were investigated through interviews with workers. The airborne radon concentration was measured in the main process areas using the RAD 7 and Raduet radon detector. Radon concentrations measured in the main process areas ranged from 16.6 to 756 Bq m-3, which is below the ICRP's reference level of 1,000 Bq m-3. The internal radiation dose due to radon inhalation ranged from 0.193 to 5.80 mSv y- 1. This is about half of the ICRP's reference level of 10 mSv y- 1 for radon inhalation. This study can be used as technical data for radiological safety management of NORM industries in Korea.