Nickel oxide nanoparticles (NiO NPs) are highly redox active nanoparticles. They can cause acute and chronic inflammation in rat lungs. Unlike the gut microbiome, the association between the lung microbiome’s role and pulmonary inflammatory response to inhaled nanoparticles remains largely unexplored. We aimed to explore the interaction between the lung microbiome and inflammatory responses in rats exposed to NiO NPs. Thirty female Wistar rats were randomly categorized into control and low- (50 cm2/rat), and high- (150 cm2/rat) dose NiO NPs exposure groups. NiO NPs were intratracheally instilled, and cytological, biochemical, proinflammatory cytokine, and lung microbiome analyses of bronchoalveolar lavage fluid were performed at 1 day and 4 weeks after instillation. NiO NPs caused a neutrophilic and lymphocytic inflammatory response in rat lung. We demonstrated that exposure to NiO NPs can alter the lung microbial composition in rats. In particular, we found that more Burkholderiales are present in the NiO NPs exposure groups than in the control group at 1 day after instillation. Dysbiosis in the lung microbiome is thought to be associated with acute lung inflammation. We also suggested that Burkholderiales may be a key biomarker associated with lung neutrophilic inflammation after NiO NPs exposure.

This study aims to evaluate the overall asbestos exposure intensity and assess the health risk to residents due to naturally occurring asbestos (NOA) near abandoned asbestos mines in South Korea. Of 38 mines, we found 19 with measured concentrations of NOA. We evaluated the average of airborne NOA concentrations according to the environmental exposure category. When evaluated regionally by dividing into two clusters, the mean concentrations in activity-based sampling (ABS) scenarios exceeded the Korean exposure limit (0.01 f/cc) in both clusters. Moreover, airborne NOA concentrations in agricultural activity (5.49 × 10−2 f/cc) and daily activity (6.95 × 10−2 f/cc) had the highest values for clusters A and B, respectively. The excess lifetime cancer risk of one region (cluster A) by the ABS scenarios did not exceed the Korean Ministry of the Environment’s criteria for soil purification (1 × 10−4). However, one of the ABS scenarios—the daily life activity of clusters centered on Chungcheongbuk-do (cluster B)—showed an exposure of 1.08 × 10−4, greater than the limit (1 × 10−4). This indicates non negligible health damage to residents living near the abandoned asbestos mines, and it is necessary to continuously monitor and clean up the asbestos contamination.

Background Indoor air pollution can cause and exacerbate asthma. We report a previously undescribed case of occupational asthma related to indoor air pollution in a worker at an indoor air gun shooting range and highlight the potential risk of developing occupational asthma in this environment. Case presentation A 31-year-old man presented with dyspnea, cough, and sputum and was diagnosed with asthma complicated by pneumonia. Objective evidence of asthma was obtained by performing a methacholine bronchial provocation test. It was suspected that the patient had occupational asthma, which began one month after changing jobs to work within the indoor air gun shooting range. The highest peak expiratory flow (PEF) diurnal variability on working days was 15%, but the highest variation was 24%, with 4 days out of 4 weeks having a variation of over 20% related to workplace exposure. Conversely, the diurnal variability on the rest days was 7%, and no day showed a variation exceeding 20%. The difference in the average PEF between working and rest days was 52 L/min. PEF deterioration during working days and improvement on rest days were noted. Conclusions The results obtained from the in-depth analysis of the PEF were adequate to diagnose the patient with occupational asthma. Exposure to indoor air pollution and lead and the patient’s atopy and allergic rhinitis may have contributed to the development of occupational asthma.

Although exposure to asbestos via various routes has been acknowledged, comprehensive exposure and risk assessment methods have not been developed at the national level. We conducted a study to reconstruct comprehensive past asbestos exposure estimations and to suggest a method to calculate the Excess Lifetime Cancer Risk (ELCR) of Koreans. The past occupational exposure reconstruction was conducted by rebuilding the previous general population job-exposure matrix (JEM). The para-occupational and household exposure estimation was based on the pooled analysis of data from other countries as well as Korea. The neighborhood exposure from occupational sources by distance was estimated by the exponential decay model. As a result, 141 JEM exposure groups across four periods including ~79, the 80s, 90s, 2000s with a ratio of 2.0:1.0:0.5:0.05 were reconstructed. The para-occupational and household exposures were 11% and 1% of the JEM respectively. The environmental exposure source concentration from outside occupational exposure was 2.5% of the inside concentration. The ratio of the concentration of environmental exposure source (C0) to distance d (Cd) was exp-kd with a decay constant k of 6.834. The mean concentrations (f/cc) were 2.28 × 10−3 for outdoor, 4.65 × 10−5 for indoor, 1.95 × 10−2 for transportation activity, 4.44 × 10−2 for agricultural activity, and 4.68 × 10−2 for daily life activity in naturally occurring asbestos areas. Indoor and outdoor asbestos concentrations from living in a slate roof house were 1.73 × 10−6 and 2.70 × 10−8, respectively. For improved generalizability, validity, and applicability of the proposed method, further studies on each route with real assessments and experiments are required.

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