Cancer risk among World Trade Center rescue and recovery workers: A review.

Twenty years after the September 11th, 2001 terrorist attacks, the association between exposures present at the World Trade Center (WTC) site and the risk of several specific types of cancer has been reported among rescue and recovery workers. The authors' objective was to conduct an updated review of these data. Most studies have found elevated rates of both prostate and thyroid cancers compared with rates in the general population, and some have reported statistically significant differences for the rates of all cancers as well. Studies including a larger combined cohort of WTC-exposed rescue and recovery workers from 3 main cohorts have since replicated findings for these cancers, with additional years of follow-up. Among this combined cohort, although a lower-than-expected standardized incidence ratio for all cancers was observed, WTC exposure was also related to an increased risk of cutaneous melanoma and tonsil cancer. Importantly, another study found that WTC-exposed rescue and recovery workers who are enrolled in the federally funded medical monitoring and treatment program experienced improved survival post-cancer diagnosis compared with New York state patients with cancer. On the basis of these combined cohort studies, the full effect of WTC exposure on cancer risk is becoming clearer. Consequently, the authors believe that surveillance of those with WTC exposure should be continued, and in-depth analysis of epidemiologic, molecular, and clinical aspects of specific cancers in these workers should be pursued.

Pediatric leukemia and maternal occupational exposure to anticancer drugs: the Japan Environment and Children's Study.

ABSTRACT: Occupational exposure to medical agents and ionizing radiation has been suggested as a possible risk factor for childhood cancer. However, the relationship between such exposure and pediatric malignant neoplasms has not yet been comprehensively studied. This cohort study aimed to investigate the association between parental occupational exposure to hazardous medical agents or ionizing radiation and the risk of childhood cancer in offspring. Data from a large birth cohort in Japan, which included 104 062 fetuses, were analyzed. The primary outcome was the development of leukemia or brain tumors diagnosed by community physicians during the first 3 years after birth. Exposure factors were medical agents, including anticancer agents, ionizing radiation, and anesthetics, handled by mothers during pregnancy or by fathers for 3 months before conception. The incidence of leukemia, but not of brain tumors, was higher in mothers exposed to anticancer drugs. Multivariable regression analysis showed that maternal exposure to anticancer drugs was associated with an increased risk of leukemia in offspring older than 1 year (adjusted relative risk, 7.99 [95% confidence interval, 1.98-32.3]). Detailed information obtained from medical certificates of patients with identified leukemia revealed no infant leukemia but acute lymphoblastic leukemias in the exposed group. Our findings suggest that maternal occupational exposure to anticancer drugs may be a potential risk factor for acute lymphoblastic leukemia in offspring older than 1 year. Effective prevention methods may be necessary to prevent maternal exposure to anticancer drugs and to reduce the risk of childhood malignant neoplasms.

Impact of Wildfires on Cardiovascular Health.

Wildfire smoke (WFS) is a mixture of respirable particulate matter, environmental gases, and other hazardous pollutants that originate from the unplanned burning of arid vegetation during wildfires. The increasing size and frequency of recent wildfires has escalated public and occupational health concerns regarding WFS inhalation, by either individuals living nearby and downstream an active fire or wildland firefighters and other workers that face unavoidable exposure because of their profession. In this review, we first synthesize current evidence from environmental, controlled, and interventional human exposure studies, to highlight positive associations between WFS inhalation and cardiovascular morbidity and mortality. Motivated by these findings, we discuss preventative measures and suggest interventions to mitigate the cardiovascular impact of wildfires. We then review animal and cell exposure studies to call attention on the pathophysiological processes that support the deterioration of cardiovascular tissues and organs in response to WFS inhalation. Acknowledging the challenges of integrating evidence across independent sources, we contextualize laboratory-scale exposure approaches according to the biological processes that they model and offer suggestions for ensuring relevance to the human condition. Noting that wildfires are significant contributors to ambient air pollution, we compare the biological responses triggered by WFS to those of other harmful pollutants. We also review evidence for how WFS inhalation may trigger mechanisms that have been proposed as mediators of adverse cardiovascular effects upon exposure to air pollution. We finally conclude by highlighting research areas that demand further consideration. Overall, we aspire for this work to serve as a catalyst for regulatory initiatives to mitigate the adverse cardiovascular effects of WFS inhalation in the community and alleviate the occupational risk in wildland firefighters.

Mesothelioma: Scientific clues for prevention, diagnosis, and therapy.

Mesothelioma affects mostly older individuals who have been occupationally exposed to asbestos. The global mesothelioma incidence and mortality rates are unknown, because data are not available from developing countries that continue to use large amounts of asbestos. The incidence rate of mesothelioma has decreased in Australia, the United States, and Western Europe, where the use of asbestos was banned or strictly regulated in the 1970s and 1980s, demonstrating the value of these preventive measures. However, in these same countries, the overall number of deaths from mesothelioma has not decreased as the size of the population and the percentage of old people have increased. Moreover, hotspots of mesothelioma may occur when carcinogenic fibers that are present in the environment are disturbed as rural areas are being developed. Novel immunohistochemical and molecular markers have improved the accuracy of diagnosis; however, about 14% (high-resource countries) to 50% (developing countries) of mesothelioma diagnoses are incorrect, resulting in inadequate treatment and complicating epidemiological studies. The discovery that germline BRCA1-asssociated protein 1 (BAP1) mutations cause mesothelioma and other cancers (BAP1 cancer syndrome) elucidated some of the key pathogenic mechanisms, and treatments targeting these molecular mechanisms and/or modulating the immune response are being tested. The role of surgery in pleural mesothelioma is controversial as it is difficult to predict who will benefit from aggressive management, even when local therapies are added to existing or novel systemic treatments. Treatment outcomes are improving, however, for peritoneal mesothelioma. Multidisciplinary international collaboration will be necessary to improve prevention, early detection, and treatment.

Occupational Benzene Exposure and Lung Cancer Risk: A Pooled Analysis of 14 Case-Control Studies.

Rationale: Benzene has been classified as carcinogenic to humans, but there is limited evidence linking benzene exposure to lung cancer. Objectives: We aimed to examine the relationship between occupational benzene exposure and lung cancer. Methods: Subjects from 14 case-control studies across Europe and Canada were pooled. We used a quantitative job-exposure matrix to estimate benzene exposure. Logistic regression models assessed lung cancer risk across different exposure indices. We adjusted for smoking and five main occupational lung carcinogens and stratified analyses by smoking status and lung cancer subtypes. Measurements and Main Results: Analyses included 28,048 subjects (12,329 cases, 15,719 control subjects). Lung cancer odds ratios ranged from 1.12 (95% confidence interval, 1.03-1.22) to 1.32 (95% confidence interval, 1.18-1.48) (Ptrend = 0.002) for groups with the lowest and highest cumulative occupational exposures, respectively, compared with unexposed subjects. We observed an increasing trend of lung cancer with longer duration of exposure (Ptrend < 0.001) and a decreasing trend with longer time since last exposure (Ptrend = 0.02). These effects were seen for all lung cancer subtypes, regardless of smoking status, and were not influenced by specific occupational groups, exposures, or studies. Conclusions: We found consistent and robust associations between different dimensions of occupational benzene exposure and lung cancer after adjusting for smoking and main occupational lung carcinogens. These associations were observed across different subgroups, including nonsmokers. Our findings support the hypothesis that occupational benzene exposure increases the risk of developing lung cancer. Consequently, there is a need to revisit published epidemiological and molecular data on the pulmonary carcinogenicity of benzene.

Increasing awareness regarding the relationship between environmental exposures and allergic disease.

This review highlights studies from the past 3 years that add to the understanding of the impact of environmental exposures on allergic disease. These include aeroallergens, air quality, prenatal or early-life exposures, and occupational exposures. Recent studies have focused on the relationship between the environment, the microbiome, and allergic disease, and new therapeutic options have also been reviewed. Lastly, there has been significant recent research improving our knowledge of the link between health disparities and environmental exposures. These scientific advances have resulted in a better understanding that sets the foundation for current and future research dedicated to improving health outcomes by modifying environmental exposures.

Creatinine clearance is maintained in a range of wet-bulb globe temperatures and work-rest ratios during simulated occupational heat stress.

We tested the hypothesis that compliance with the National Institute for Occupational Safety and Health (NIOSH) heat stress recommendations will prevent reductions in glomerular filtration rate (GFR) across a range of wet-bulb globe temperatures (WBGTs) and work-rest ratios at a fixed work intensity. We also tested the hypothesis that noncompliance would result in a reduction in GFR compared with a work-rest matched compliant trial. Twelve healthy adults completed five trials (four NIOSH compliant and one noncompliant) that consisted of 4 h of exposure to a range of WBGTs. Subjects walked on a treadmill (heat production: approximately 430 W) and work-rest ratios (work/h: 60, 45, 30, and 15 min) were prescribed as a function of WBGT (24°C, 26.5°C, 28.5°C, 30°C, and 36°C), and subjects drank a sport drink ad libitum. Peak core temperature (TC) and percentage change in body weight (%ΔBW) were measured. Creatinine clearance measured pre- and postexposure provided a primary marker of GFR. Peak TC did not differ among NIOSH-compliant trials (P = 0.065) but differed between compliant versus noncompliant trials (P < 0.001). %ΔBW did not differ among NIOSH-compliant trials (P = 0.131) or between compliant versus noncompliant trials (P = 0.185). Creatinine clearance did not change or differ among compliant trials (P ≥ 0.079). Creatinine clearance did not change or differ between compliant versus noncompliant trials (P ≥ 0.661). Compliance with the NIOSH recommendations maintained GFR. Surprisingly, despite a greater heat strain in a noncompliant trial, GFR was maintained highlighting the potential relative importance of hydration.NEW & NOTEWORTHY We highlight that glomerular filtration rate (GFR) is maintained during simulated occupational heat stress across a range of total work, work-rest ratios, and wet-bulb globe temperatures with ad libitum consumption of an electrolyte and sugar-containing sports drink. Compared with a work-rest matched compliant trial, noncompliance resulted in augmented heat strain but did not induce a reduction in GFR likely due to an increased relative fluid intake and robust fluid conservatory responses.

Occupational asbestos exposure and risk of esophageal cancer: A systematic review and meta-analysis.

Esophageal cancer (EC), which includes squamous cell carcinoma (ESCC) and adenocarcinoma (EAC), is an important cancer with poor prognosis and high mortality rate. Several occupational exposures have been associated with EC. We aim to investigate the association between occupational asbestos exposure and EC risk, considering types of asbestos and histology of the disease. We included studies mentioned in the list of references in previous reviews and pooled analyses, and we conducted an independent search in PubMed and Scopus. Forest plots of relative risks (RR) were constructed based on the association between occupational asbestos and EC risk. Random-effects models were used to address heterogeneity between 48 independent cohort and case-control studies. We found an association between occupational asbestos exposure and EC (meta-relative risk [RR] = 1.20, 95% confidence interval [CI] = 1.09-1.32; I2 = 58.8%, p-heterogeneity [het] <.001). The results of stratification by job (p-het = .20) indicate an increased RR among asbestos product workers (RR = 1.39, 95% CI = 1.07-1.81), asbestos applicators (RR = 1.41, 95% CI = 1.20-1.67), and construction workers (RR = 1.12, 95% CI = 1.02-1.24). There was no heterogeneity in meta-RR according to outcome (p = .29), geographic region (p = .69), year of publication (p = .59), quality score (p = .73), asbestos type (p = .93), study design (p = .87), and gender (p = .88), control for potential confounders (p = .20), year of first employment (p = .94) and exposure level (p = .43). The stratification analysis by histology type found an increased RR for both ESCC 1.33(1.03-1.71) and EAC 1.45(1.03-2.04) (p-het = .68). We didn't find evidence of publication bias (p = .07). The results of our study suggest that occupational asbestos exposure is associated with an increased risk of EC in both histology types.

Occupational exposure to benzene and risk of non-Hodgkin lymphoma in an extended follow-up of two population-based prospective cohorts of Chinese men and women.

The carcinogenicity of benzene was reevaluated by the International Agency for Research on Cancer in 2017, with the Working Group reaffirming positive yet inconclusive associations with non-Hodgkin lymphoma (NHL). To extend our previous observation of a significant exposure-response for cumulative occupational benzene exposure and NHL risk among Chinese women in a population-based cohort in Shanghai, we extended follow-up of this cohort and pooled the data with a similarly designed population-based cohort of men in Shanghai. Cumulative exposure estimates were derived for 134,449 participants in the pooled analysis by combining ordinal job-exposure matrix intensity ratings with quantitative benzene measurements from an inspection database of Shanghai factories. Associations between benzene exposure metrics and NHL (n = 363 cases including multiple myeloma [MM]) were assessed using Cox proportional hazard models. Ever occupational exposure to benzene in the pooled population was associated with NHL risk (HR = 1.5, 95% CI = 1.2-2.0), and exposure-response relationships were observed for increasing duration (ptrend = .003) and cumulative exposure (ptrend = .003). Associations with ever exposure, duration, and cumulative exposure were similar for NHL with and without MM in the case definition, including lifetime cumulative exposures in the highest quartile (HR = 1.6, 95% CI = 1.1-2.4 with MM included; HR = 1.7, 95% CI = 1.1-2.7 with MM excluded). An elevated risk of the chronic lymphocytic leukemia subtype was suggested in the pooled analyses (HR for ever vs. never exposure = 2.3, 95% CI = 0.9-5.6). These observations provide additional support for a plausible association between occupational benzene exposure and risk of NHL.

Artificial stone silicosis: a UK case series.

Silicosis due to artificial stone (AS) has emerged over the last decade as an increasing global issue. We report the first eight UK cases. All were men; median age was 34 years (range 27-56) and median stone dust exposure was 12.5 years (range 4-40) but in 4 cases was 4-8 years. One is deceased; two were referred for lung transplant assessment. All cases were dry cutting and polishing AS worktops with inadequate safety measures. Clinical features of silicosis can closely mimic sarcoidosis. UK cases are likely to increase, with urgent action needed to identify cases and enforce regulations.

Relationship between cumulative silica exposure and silicosis: a systematic review and dose-response meta-analysis.

BACKGROUND: Silicosis, a chronic respiratory disease caused by crystalline silica exposure, is a persistent global lung health issue. No systematic review of the relationship between cumulative respirable crystalline silica (RCS) exposure and silicosis exists. UK exposure limits are currently under review. We therefore performed a systematic review and dose-response meta-analysis of this relationship. METHODS: Web of Science, Medline and Embase were searched on 24 February 2023. Studies of radiographic, autopsy or death certificate silicosis, with an estimated average follow-up of over 20 years since first employment, were included. Cumulative silicosis risk methods were compared. The relative risks (RR) of silicosis at increasing cumulative exposures were calculated and used to estimate the absolute risk reduction (ARR). RESULTS: Eight eligible studies, including 10 cohorts, contributed 8792 cases of silicosis among 65 977 participants. Substantial differences in cumulative risk estimates between methodologies exist. Using the same method, we observed higher cumulative silicosis risks among mining compared with non-mining cohorts. A reduction from 4 to 2 mg/m³-years in cumulative RCS exposure corresponded to substantial risk reductions among miners (RR 0.23 (95% CI 0.18 to 0.29, I2=92.9%) with an ARR of 323 (95% CI 298 to 344) per 1000) and non-miners (RR 0.55 (95% CI 0.36 to 0.83, I2=77.0%) with an ARR of 23 (95% CI 9 to 33) per 1000). CONCLUSION: Despite significant heterogeneity, our findings support a reduction in permissible exposure limits from 0.1 mg/m3 to 0.05 mg/m³, particularly among mining populations. Further research is needed among non-miners as only two studies were eligible.

Risk of hypersensitivity pneumonitis and other interstitial lung diseases following organic dust exposure.

BACKGROUND: Organic dust is associated with hypersensitivity pneumonitis, and associations with other types of interstitial lung disease (ILD) have been suggested. We examined the association between occupational organic dust exposure and hypersensitivity pneumonitis and other ILDs in a cohort study. METHODS: The study population included all residents of Denmark born in 1956 or later with at least 1 year of gainful employment since 1976. Incident cases of hypersensitivity pneumonitis and other ILDs were identified in the Danish National Patient Register 1994-2015. Job exposure matrices were used to assign individual annual levels of exposure to organic dust, endotoxin and wood dust from 1976 to 2015. We analysed exposure-response relations by different exposure metrics using a discrete-time hazard model. RESULTS: For organic dust, we observed increasing risk with increasing cumulative exposure with incidence rate ratios (IRR) per 10 unit-years of 1.19 (95% CI 1.12 to 1.27) for hypersensitivity pneumonitis and 1.04 (95% CI 1.02 to 1.06) for other ILDs. We found increasing risk with increasing cumulative endotoxin exposure for hypersensitivity pneumonitis and other ILDs with IRRs per 5000 endotoxin units/m3-years of 1.55 (95% CI 1.38 to 1.73) and 1.09 (95% CI 1.00 to 1.19), respectively. For both exposures, risk also increased with increasing duration of exposure and recent exposure. No increased risks were observed for wood dust exposure. CONCLUSION: Exposure-response relations were observed between organic dust and endotoxin exposure and hypersensitivity pneumonitis and other ILDs, with lower risk estimates for the latter. The findings indicate that organic dust should be considered a possible cause of any ILD. TRIAL REGISTRATION NUMBER: j.no.: 1-16-02-196-17.

Extreme Heat and Occupational Health Risks.

Climate change poses a significant occupational health hazard. Rising temperatures and more frequent heat waves are expected to cause increasing heat-related morbidity and mortality for workers across the globe. Agricultural, construction, military, firefighting, mining, and manufacturing workers are at particularly high risk for heat-related illness (HRI). Various factors, including ambient temperatures, personal protective equipment, work arrangements, physical exertion, and work with heavy equipment may put workers at higher risk for HRI. While extreme heat will impact workers across the world, workers in low- and middle-income countries will be disproportionately affected. Tracking occupational HRI will be critical to informing prevention and mitigation strategies. Renewed investment in these strategies, including workplace heat prevention programs and regulatory standards for indoor and outdoor workers, will be needed. Additional research is needed to evaluate the effectiveness of interventions in order to successfully reduce the risk of HRI in the workplace.

The addition of a leaded arm sleeve to leaded aprons further decreases operator upper outer quadrant chest wall radiation dose during fluoroscopically guided interventions.

OBJECTIVE: Breast cancer most commonly occurs in the upper outer quadrant (UOQ) chest wall (CW). The effectiveness of routine leaded aprons to protect this region of the body in interventionalists during fluoroscopically guided interventions (FGIs) is unknown. Given the high lifetime attributable risks of prolonged occupational exposure to ionizing radiation and the increasing number of practicing female vascular surgeons and interventionalists, we sought to determine if the use of a leaded arm shield would offer additional protection to the lateral CW and axilla in operators compared with routine leaded aprons. METHODS: Effectiveness of leaded sleeves in attenuating radiation dose to the axilla and UOQ was evaluated in clinical practice and simulated scenarios. In the clinical setting, optically stimulated luminescence nanoDot detectors were placed at the UOQ lateral CW position, both over and under a standard leaded apron vest with and without the addition of an antimony/bismuth Enviro-Lite sleeve on two vascular surgeons performing FGIs. In the simulation, nanoDots were similarly placed on an anthropomorphic phantom positioned to represent a primary operator performing right femoral access. Fluorography was performed on 12-inch-thick acrylic scatter phantom at 80 kVp for an exposure of 3 Gy reference air kerma. Experiments were done with and without the sleeve. Paired Wilcoxon and χ2 tests were performed to identify the statistical significance of radiation attenuation. RESULTS: Operator UOQ CW dose was measured during 61 FGIs: 33 cases (54%) with and 28 cases (46%) without the sleeve. Median procedure reference air kerma and fluoroscopy time was 180 mGy (interquartile range [IQR], 85-447 mGy) and 21 minutes (IQR, 11-39 minutes) when the sleeve was worn vs 100 mGy (IQR, 67-270 mGy) and 11 minutes (IQR, 6.3-25 minutes) without the sleeve. Radiation dose to the operator's UOQ was reduced by 96% (IQR, 85%-96%) when the sleeve was present and by 62% (IQR, 44%-82%; P < .001) without the sleeve. In the simulated setting, the sleeve reduced the radiation dose to the UOQ compared with the apron alone (96% vs 67%; P < .001). CONCLUSIONS: Routine leaded aprons do attenuate the majority of UOQ chest wall radiation dose; however, the addition of a lead-equivalent sleeve further significantly reduces this dose. Because this area of the body has a high incidence of cancer formation, additional protection, especially to female interventionalists, seems prudent. Vascular surgeons should consider using a protective sleeve with their personal protective equipment when performing complex fluoroscopically guided procedures.

A procedural step analysis of radiation exposure in fenestrated endovascular aortic repair.

OBJECTIVE: Radiation exposure during complex endovascular aortic repair may be associated with tangible adverse effects in patients and operators. This study aimed to identify the steps of highest radiation exposure during fenestrated endovascular aortic repair (FEVAR) and to investigate potential intraoperative factors affecting radiation exposure. METHODS: Prospective data of 31 consecutive patients managed exclusively with four-fenestration endografts between March 1, 2020, and July 1, 2022 were retrospectively analyzed. Leveraging the conformity of the applied technique, every FEVAR operation was considered a combination of six overall stages composed of 28 standardized steps. Intraoperative parameters, including air kerma, dose area product, fluoroscopy time, and number of digital subtraction angiographies (DSAs) and average angulations were collected and analyzed for each step. RESULTS: The mean procedure duration and fluoroscopy time was 140 minutes (standard deviation [SD], 32 minutes), and 40 minutes (SD, 9.1 minutes), respectively. The mean air kerma was 814 mGy (SD, 498 mGy), and the mean dose area product was 66.8 Gy cm2 (SD, 33 Gy cm2). The percentage of air kerma of the entire procedure was distributed throughout the following procedure stages: preparation (13.9%), main body (9.6%), target vessel cannulation (27.8%), stent deployment (29.1%), distal aortoiliac grafting (14.3%), and completion (5.3%). DSAs represented 23.0% of the total air kerma. Target vessel cannulation and stent deployment presented the highest mean lateral angulation (67 and 63 degrees, respectively). Using linear regression, each minute of continuous fluoroscopy added 18.9 mGy of air kerma (95% confidence interval, 17.6-20.2 mGy), and each DSA series added 21.1 mGy of air kerma (95% confidence interval, 17.9-24.3 mGy). Body mass index and lateral angulation were significantly associated with increased air kerma (P < .001). CONCLUSIONS: Cannulation of target vessels and bridging stent deployment are the steps requiring the highest radiation exposure during FEVAR cases. Optimized operator protection during these steps is mandatory.

Effect of Pb-exposure and B vitamin deficiencies on δ-aminolevulinic acid dehydratase activity among workers from Pb recycling plants.

Previous studies reported that Pb exposure causes a negative association with delta-aminolevulinic acid dehydratase activity (δ-ALAD), but the impact of Pb exposure (dose and time), B vitamin deficiencies, and lifestyle factors needs to be explored. In this study, the impact of Pb exposure, B vitamin deficiencies, and lifestyle factors on δ-ALAD activity among workers exposed to Pb from the Pb-recycling process was evaluated. Blood lead levels (BLLs), B vitamins (B6, B9, and B12), hematological factors (Hb% and HCT), lifestyle factors, and δ-ALAD activity was assessed in 170 male Pb-exposed workers engaged in the Pb recycling process. BLLs are estimated using the ICP-OES method. B vitamins in serum samples from workers were determined using the ELISA method. The δ-ALAD activity in whole blood samples was determined using the spectrophotometer method. The lifestyle factors were collected using a standard questionnaire. The δ-ALAD activity was significantly decreased in workers with the habits of alcohol use, tobacco consumption, hematocrit < 41%, mild and moderate categories of anemia, vitamin B6 and B12 deficiency, and BLL categories of 10-30, 30-50, and > 50 µg/dL. Multiple regression analysis revealed that the independent variables of alcohol consumption (ß = - 0.170; P = 0.025), BLLs (ß = - 0.589; P = 0.001) and Hb% (ß = 0.183; P = 0.001) significantly influenced the δ-ALAD activity with 44.2% (R2 = 0.442). Among the workers exposed to Pb from the Pb recycling plant, δ-ALAD activity was considerably reduced by Pb exposure, B vitamin deficiency, hematological parameters, and lifestyle factors.

Extracellular vesicles-derived long noncoding RNAs participated in benzene hematotoxicity by mediating apoptosis and autophagy.

Benzene is a common contaminant in the workplace and wider environment, which induces hematotoxicity. Our previous study has implicated that lncRNAs mediated apoptosis and autophagy induced by benzene. Nevertheless, the roles of extracellular vesicle(EVs)-derived lncRNAs in benzene toxicity are unknown. However, the role of EVs and EVs-derived lncRNAs in benzene-induced toxicity remains unclear. In this research, we explored the function of EVs and EVs-derived lncRNAs in cell-cell communication through benzene-induced apoptosis and autophagy. Our findings demonstrated that EVs derived from 1,4-BQ-treated cells treated cells and coculture with 1,4-BQ-treated cells enhanced apoptosis and autophagy via regulating the pathways of PI3K-AKT-mTOR and chaperone-mediated autophagy. Treating with GW4869 in 1,4-BQ-treated cells significantly inhibited EV secretion, which reduced apoptosis and autophagy. Furthermore, we identified a set of differentially expressed autophagy- and apoptosis-related lncRNAs using EVs-derived lncRNA sequencing. Among them, 8 candidate lncRNAs were upregulated in EVs derived from 1,4-BQ-treated cells, as determined by lncRNA sequencing and qRT-PCR. Importantly, these lncRNAs were also increased in the serum EVs of benzene-exposed workers. 1,4-BQ-treated cells released EVs that transfer differentially expressed lncRNAs, thereby inducing apoptosis and autophagy in the recipient cells. The above results support the hypothesis that EVs-derived lncRNAs participate in intercellular communication during benzene-induced hematotoxicity and function as potential biomarkers for risk assessment of benzene-exposed workers.

Development and evaluation of a questionnaire to capture environmental and occupational inhalational exposures in adults with fibrotic interstitial lung disease.

BACKGROUND: Identification of exposures in patients with interstitial lung diseases (ILDs) is essential for diagnosis and management and can be facilitated through the use of exposure questionnaires. However, for most ILDs, a patient-focused questionnaire is lacking. Cognitive interviewing is a methodology used to evaluate sources of understanding and misunderstanding in a questionnaire and to provide evidence of content validity. We developed and refined a new exposure questionnaire for patients with fibrotic ILDs by using cognitive interviewing to establish its understandability and content validity. METHODS: An exposure assessment questionnaire was developed by a multidisciplinary team. Cognitive interviews with 24 patients with fibrosing ILDs were conducted by trained interviewers over the phone or Zoom using a semi-structured interview guide. The questionnaire was amended based on the interviewers' interpretation of sources of misunderstanding. The revised questionnaire was tested in a second round of cognitive interviews with a different group of 24 patients. RESULTS: Among the 48 patients who completed interviews, mean age was 61 years, 58.3% were male and 75.0% were white. Based on the first round of cognitive interviews, the multidisciplinary team modified the questions, organization, and instructions of the questionnaire to facilitate recall, adjust for exposures that were frequently misunderstood or required clarification, and focus on clinically relevant exposures. The revised questionnaire performed well in the second round of interviews. CONCLUSION: An exposure questionnaire, developed with input from patients, can be used to assess clinically relevant exposures in adults with fibrosing ILDs. This is the first questionnaire for all types of fibrosing ILD to have undergone content validation.

Chronic diesel exhaust exposure induced pulmonary vascular remodeling a potential trajectory for traffic related pulmonary hypertension.

BACKGROUND: As one of the most common traffic-related pollutants, diesel exhaust (DE) confers high risk for cardiovascular and respiratory diseases. However, its impact on pulmonary vessels is still unclear. METHODS: To explore the effects of DE exposure on pulmonary vascular remodeling, our study analyzed the number and volume of small pulmonary vessels in the diesel engine testers (the DET group) from Luoyang Diesel Engine Factory and the controls (the non-DET group) from the local water company, using spirometry and carbon content in airway macrophage (CCAM) in sputum. And then we constructed a rat model of chronic DE exposure, in which 12 rats were divided into the DE group (6 rats with 16-week DE exposure) and the control group (6 rats with 16-week clean air exposure). During right heart catheterization, right ventricular systolic pressure (RVSP) was assessed by manometry. Macrophage migration inhibitory factor (MIF) in lung tissues and bronchoalveolar lavage fluid (BALF) were measured by qRT-PCR and ELISA, respectively. Histopathological analysis for cardiovascular remodeling was also performed. RESULTS: In DET cohort, the number and volume of small pulmonary vessels in CT were positively correlated with CCAM in sputum (P<0.05). Rat model revealed that chronic DE-exposed rats had elevated RVSP, along with increased wall thickness of pulmonary small vessels and right the ventricle. What's more, the MIF levels in BALF and lung tissues were higher in DE-exposed rats than the controls. CONCLUSION: Apart from airway remodeling, DE also induces pulmonary vascular remodeling, which will lead to cardiopulmonary dysfunction.

Shedding light on occupational exposure to the sun.

Roughly one in three non-melanoma skin cancer deaths worldwide is associated with working outdoors in the sun. Gary Humphreys reports.