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OBJECTIVES: This study aims to assess the specific PM2.5-bound metallic elements that contribute to asthma emergency department visits by using a case-crossover study design. METHODS: This study analyzed data from 11,410 asthma emergency department visits as case group and 22,820 non-asthma onset dates occurring one week and two weeks preceding the case day as controls from 2017 to 2020. PM2.5 monitoring data and 35 PM.2.5-bound metallic elements from six different regions in Taiwan were collected. Conditional logistic regression models were used to assess the relationship between asthma and PM2.5-bound metallic elements. RESULTS: Our investigation revealed a statistically significant risk of asthma emergency department visits associated with PM2.5 exposure at lag 0, 1, 2, and 3 during autumn. Additionally, PM2.5-bound hafnium (Hf), thallium (Tl), rubidium (Rb), and aluminum (Al) exhibited a consistently significant positive correlation with asthma emergency department visits at lags 1, 2, and 3. In stratified analyses by area, age, and sex, PM2.5-bound Hf showed a significant and consistent correlation. CONCLUSIONS: This study provides evidence of PM2.5-bound metallic elements effects in asthma exacerbations, particularly for Hf. It emphasizes the importance of understanding the origins of these metallic elements and pursuing emission reductions to mitigate regional health risks.
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Poluentes Atmosféricos , Asma , Estudos Cross-Over , Serviço Hospitalar de Emergência , Material Particulado , Asma/epidemiologia , Asma/induzido quimicamente , Taiwan/epidemiologia , Serviço Hospitalar de Emergência/estatística & dados numéricos , Material Particulado/análise , Humanos , Masculino , Feminino , Pessoa de Meia-Idade , Adulto , Poluentes Atmosféricos/análise , Idoso , Adolescente , Adulto Jovem , Metais/análise , Criança , Exposição Ambiental/efeitos adversos , Pré-Escolar , Lactente , Visitas ao Pronto SocorroRESUMO
OBJECTIVE: Exposure to ambient PM2.5 and its bound metals poses a risk to health and disease, via, in part, oxidative stress response. A variety of oxidative stress markers have been used as markers of response, but their relevance to environmental exposure remains to be established. We evaluated, longitudinally, a battery of oxidative stress markers and their relationship with the exposure of PM2.5 and its bound metals in a panel of healthy participants. MATERIAL AND METHODS: Levels of residence- and personal-based ambient air PM2.5 and its bound metals, as well as of lung function parameters, were assessed in a total of 58 questionnaire-administered healthy never smoker participants (male, 39.7%). Levels of urinary oxidative stress markers, including Nε-(hexanoyl)-lysine (HEL; an early lipid peroxidation product), 4-hydroxynonenal (4-HNE), N7-methylguanine (N7-meG), and 8-hydroxy-2-deoxyguanosine (8-OHdG), plasma antioxidants [superoxide dismutase (SOD) and glutathione peroxidase (GPx), and urinary metals were measured by ELISA, LC-MS, and ICP-MS, respectively. The results of three repeated measurements at two-month intervals were analyzed using the Generalized Estimating Equation (GEE). RESULTS: After adjusting for confounders, residence- and personal-based PM2.5 levels were positively associated with HEL (ß = 0.22 and 0.18) and N7-meG (ß = 0.39 and 0.13). Significant correlations were observed between personal air PM2.5-Pb and urinary Pb with HEL (ß = 0.08 and 0.26). While FVC, FEV1, FEV1/FVC, MMF, and PEFR predicted% were normal, a negative interaction (pollutant*time, P < 0.05) was noted for PM2.5-V, Mn, Co, Ni, Zn, As, and Pb. Additionally, a negative interaction was found for N7-meG (ß = -21.35, -18.77, -23.86) and SOD (ß = -26.56, -26.18, -16.48) with FEV1, FVC, and PEFR predicted%, respectively. CONCLUSION: These findings emphasize potential links between environmental exposure, internal dose, and health effects, thereby offering valuable markers for future research on metal exposure, oxidative stress, and health outcomes.
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Poluentes Atmosféricos , Humanos , Masculino , Poluentes Atmosféricos/análise , Material Particulado/análise , Voluntários Saudáveis , Chumbo/análise , Exposição Ambiental/análise , Estresse Oxidativo , Superóxido DismutaseRESUMO
OBJECTIVE: The purpose of this study was to assess cancer risk among agricultural workers compared to the general population. METHODS: The study utilized data from Farmers' Health Insurance (FHI) in Taiwan, which enrolled agricultural workers (N=1 175 149). The enrolled workers were matched to a general population (N=1 175 149) of the same age, gender, township, and enrollment year. The study population was linked to the National Cancer Registry to identify new cancer cases between 2000 and 2018. The Cox proportional hazards model was used to estimate the hazard ratio and 95% confidence interval for outcomes. RESULTS: During the study period, 136 913 new cancers among agricultural workers were identified. The study found that male farmers had an increased cancer risk, including lymphocytic leukemia, chronic myelogenous leukemia, non-Hodgkin's lymphoma (NHL), oral cancer, lip cancer, esophagus cancer, rectum and rectosigmoid junction cancer, liver and intrahepatic bile duct cancer, lung cancer, trachea and bronchi cancer, and other non-melanoma skin cancer, even when considering the latency period. Female farmers had an elevated risk of multiple myeloma and other non-melanoma skin cancer. Moreover, only lymphoma, NHL, other lymphoid, and multiple myeloma, were both found to occur at different insurance periods. CONCLUSIONS: This study provides farmer cancer patterns and risk, adding to the evidence that farmers are at increased risk of certain types of cancer, especially for hematological cancers. As exposure varies by farm operation type, individual farmer exposure may vary widely. Further understanding of the complex relationship between occupational exposure, environmental factors, and lifestyle factors is needed.
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Doenças dos Trabalhadores Agrícolas , Linfoma não Hodgkin , Mieloma Múltiplo , Exposição Ocupacional , Neoplasias Cutâneas , Humanos , Masculino , Feminino , Fazendeiros , Estudos de Coortes , Taiwan/epidemiologia , Linfoma não Hodgkin/epidemiologia , Neoplasias Cutâneas/complicações , Exposição Ocupacional/efeitos adversos , Fatores de Risco , Doenças dos Trabalhadores Agrícolas/epidemiologia , Doenças dos Trabalhadores Agrícolas/etiologiaRESUMO
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Indium tin oxide exposure poses a potential health risk, but the exposure assessment in occupational setting remains incomplete and continues to be a significant challenge. To this end, we investigated the association of work type, airborne indium concentration, respirable fraction of total indium, and cumulative indium exposure index (CEI) with the levels of plasma indium (P-In) and urinary indium (U-In) among 302 indium tin oxide target manufacturing and recycling workers in Taiwan. We observed that recycling-crushing produced the highest concentrations of total indium (area: 2084.8 µg/m3; personal: 3494.5 µg/m3) and respirable indium (area: 533.4 µg/m3; personal: 742.0 µg/m3). Powdering produced the highest respirable fraction of total indium (area: 58.6%; personal: 81.5%), where the workers had the highest levels of P-In (geometric mean: 2.0 µg/L) and U-In (1.0 µg/g creatinine). After adjusting for the confounder, the CEIs of powdering (ßPR = 0.78; ßPR = 0.44), bonding (ßPT = 0.61; ßPT = 0.37), and processing workers (ßPT = 0.43; ßPT = 0.28) showed significant associations with P-In and U-In, validating its utility in monitoring the exposure. Also, the respirable fraction of total indium significantly contributed to the increased levels of P-In and U-In among workers. The varying levels of relationship noted between indium exposure and the levels of P-In and U-In among workers with different work types suggested that setting the exposure limits among different work types is warranted.
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Exposição Ocupacional , Humanos , Índio/análise , Exposição Ocupacional/análise , Taiwan , Compostos de Estanho/análiseRESUMO
Oxidative stress plays a crucial role in the development of diseases induced by welding fumes. To our knowledge, little information is available on the relationship between multiple heavy metal exposure and oxidative stress in welders. We assessed the relationship between multiple heavy metal exposure and oxidative damage by analyzing 174 nonsmoking male welders in a shipyard. Urinary metals were used as the internal dose of exposure to metals in welding fumes, and urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) was used as an oxidative DNA damage marker. The relationship between workers' metal levels and 8-OHdG was estimated using a multiple linear regression model. The geometric mean levels of urinary chromium (Cr), nickel (Ni), cadmium (Cd), and lead (Pb) were considerably higher in welders than in controls. Urinary Cr and Ni were determined as effective predictors of urinary 8-OHdG levels after adjusting for covariates. Oxidative DNA damage was associated with both Cr and Ni of welding fume exposure in shipyard welders (Ln Cr: ß = 0.33, 95%C.I. = 0.16-0.49; Ln Ni: ß = 0.27, 95%C.I. = 0.12-0.43). In this study, we investigated the significantly positive relationship between urinary metals (especially Cr and Ni) and 8-OHdG in nonsmoking shipyard welders. Moreover, the use of particulate respirators did not reduce metal exposure and oxidative damage. Therefore, we infer that hazard identification for welders should be conducted.
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8-Hidroxi-2'-Desoxiguanosina/análise , Poluentes Ocupacionais do Ar/toxicidade , Metais Pesados/toxicidade , Exposição Ocupacional/análise , Soldagem , Poluentes Ocupacionais do Ar/análise , Biomarcadores/urina , Dano ao DNA , Humanos , Modelos Lineares , Masculino , Metais Pesados/análise , Pessoa de Meia-Idade , Estresse OxidativoRESUMO
Sleep disorders may pose a risk to workers in the workplace. We aimed to investigate the associations between metal fume fine particulate matter (PM2.5) and sleep quality in workers. We assessed the effects of personal exposure to metal fume PM2.5 on lung functions, urinary biomarkers, and sleep quality in shipyard welding workers. In total, 96 welding workers and 54 office workers were recruited in the present study; office workers were exposed to 82.1 ± 94.1 µg/m3 PM2.5 and welding workers were exposed to 2166.5 ± 3149.1 µg/m3. Welding workers had significantly lower levels of FEV25-75 than office workers (p < 0.05). An increase in 1 µg/m3 PM2.5 was associated with a decrease of 0.003 ng/mL in urinary serotonin (95% CI = -0.007-0.000, p < 0.05) in all workers and with a decrease of 0.001 ng/mL in serotonin (95% CI = -0.004-0.002, p < 0.05) in welding workers, but these were not observed in office workers. There was no significant association of PM2.5 with urinary cortisol observed in any workers. Urinary serotonin was associated with urinary Cu, Mn, Co, Ni, Cd, and Pb. Urinary cortisol was associated with Cu, Mn, Co, Ni, Cd, and Pb. Sixteen subjects were randomly selected from each of the office and welding workers for personal monitoring of sleep quality using a wearable device. We observed that welding workers had greater awake times than did office workers (p < 0.05). Our study observed that exposure to heavy metals in metal fume PM2.5 may disrupt sleep quality in welding workers.
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Poluentes Ocupacionais do Ar/análise , Metais Pesados/análise , Exposição Ocupacional/estatística & dados numéricos , Material Particulado/análise , Soldagem/estatística & dados numéricos , Adulto , Biomarcadores/metabolismo , Gases , Humanos , Pulmão/química , Masculino , Exposição Ocupacional/análiseRESUMO
An increased understanding is needed of the physiological effects and plausible biological mechanisms that link PM2.5 (particulate matter with an aerodynamic diameter below 2.5µm) exposure to mortality and morbidities such as atherosclerosis and respiratory disease. PM2.5 causes carcinogenic health effects. Biomonitoring in humans has suggested that 8-oxo-7, 8-dihydro-2-deoxyguanosine (8-oxodG) and N7-methylguanine (N7-MeG) are correlated with oxidative and methylated DNA damage. Thus, it is meaningful to explore the mechanisms of mutagenesis and carcinogenesis associated with oxidative and methylated DNA damage by simultaneously measuring these two markers. We recruited 72 participants from 2 areas (residential and commercial as well as residential and industrial) in the greater Taipei metropolitan area at baseline. Personal samplers were used to collect 24-hour PM2.5-integrated samples. All participants completed an interview, and blood and urine samples were collected the next morning. All collection procedures were repeated twice after a two-month follow-up period. Urinary 8-oxodG and N7-MeG were assayed as biomarkers of oxidative and methylated DNA damage, respectively. Plasma superoxide dismutase (SOD) and glutathione peroxidase-1 (GPX-1) were measured as biomarkers of antioxidants. Urinary 1-hydroxypyrene (1-OHP) was used as a biomarker of exposure to polycyclic aromatic hydrocarbons (PAHs). The mean PM2.5 level was 37.3µg/m3 at baseline. PM2.5 concentrations were higher during winter than during spring and summer. After adjusting for confounds through a generalized estimating equation (GEE) analysis, N7-MeG was significantly increased by 8.1% (ß=0.034, 95% CIs=0.001-0.068) per 10µg/m3 increment in PM2.5. 8-oxodG levels were positively correlated with N7-MeG according to both cross-sectional and longitudinal analyses, and 1-OHP was significantly associated with increasing 8-oxodG and N7-MeG concentrations. Exposure to PM2.5 increases methylated DNA damage. The mean level of urinary N7-MeG was 1000-fold higher than that of 8-oxodG.