The study’s abstract reports that 108 samples, or 4.43%, met the predefined positivity threshold for H5N6, while 107, or 4.39%, met the threshold for H9N2. During 2018–2020, 25 of 914 samples (2.74%) met the threshold for H7N9. From 2021 through 2025, 22 of 1,523 samples (1.44%) met the threshold for H3N8, including nine of 100 samples collected in Nanchang in the 2024 surveillance year (9.00%). Four of 1,523 samples (0.26%) met the threshold for H10N3, and all four were from Jiujiang in 2024. For H5N8, four of 314 samples (1.27%) met the threshold in 2020. None of the 600 samples tested for H5N1 in the 2024 and 2025 surveillance years met its predefined threshold.

Samples were collected annually during winter and spring at surveillance sites in Nanchang County and in Duchang and Wuning counties, Jiujiang, Jiangxi Province. The National Influenza Center performed hemagglutination-inhibition assays using test antigens representing H5N6, H9N2, H7N9, H3N8, H10N3, H5N8 and H5N1. Positivity was defined as a titre of at least 1:20 for H3N8, H5N8, H5N1, H7N9 and H10N3, and at least 1:40 for H5N6 and H9N2. The abstract identifies peaks in H5N6 positivity in Jiujiang in 2021 and Nanchang in 2022, and in H9N2 positivity in Jiujiang in 2021 and Nanchang in 2023. It also identifies the H3N8 finding in Nanchang and the H10N3 finding in Jiujiang in the 2024 surveillance year as warranting further investigation.

Because this was an observational, cross-sectional study, the results describe antibody reactivity among selected occupationally exposed participants rather than clinically diagnosed infections. The number of samples tested differed among subtypes, locations and years, limiting direct comparisons across those groups. The article is presented in an accepted, citable version that the publisher says may undergo further edits before replacement by the final Version of Record. The authors concluded that continued serological surveillance, interpreted alongside poultry and environmental virological data, may inform risk assessment.

Subject of Research: Serological surveillance of avian influenza antibodies among poultry-exposed populations around Poyang Lake, China

Article Title: 2018–2025 Serological study on avian influenza among occupationally exposed populations in the Poyang Lake area — the region with the highest environmental surveillance positive rate in China

Article References: Nie, C., Li, Y., Xie, W., Qian, K., Xu, T., He, F., Deng, Z., Wei, W., Hou, Y., Tu, X., Xiang, T., & Song, W. (2026). 2018–2025 Serological study on avian influenza among occupationally exposed populations in the Poyang Lake area — the region with the highest environmental surveillance positive rate in China. BMC Public Health. https://doi.org/10.1186/s12889-026-29921-6

Image Credits: AI Generated

DOI: 10.1186/s12889-026-29921-6

Keywords: avian influenza, serological surveillance, Poyang Lake, hemagglutination inhibition, occupational exposure, poultry workers, H5N6, H9N2, H3N8, H10N3, Jiangxi, China

Researchers retained the most recent eligible screening encounter for each participating miner, providing current information on age, underground mining tenure, region, occupational history and radiographic classification. They excluded unreadable radiographs, records from retired miners and miners with any surface-mining experience, leaving 30,319 miners whose recorded experience was underground. The sample was overwhelmingly male, with 98.9% identifying as men, and 94.6% identifying as White. Among participants who reported ethnicity, 10.0% identified as Hispanic. At their most recent encounter, miners had a median age of 44 years and a median underground tenure of 17 years.

Miners were classified as having coal workers’ pneumoconiosis when chest radiographs showed small opacities at an International Labour Organization profusion of at least 1/0. Progressive massive fibrosis was identified through large opacities exceeding 1 cm. Occupational histories were collected with a standardized federal questionnaire, usually at screening encounters occurring every three to five years. Miners reported the jobs they had held during their careers, and each occupation category was recorded as “ever” or “never.” Because job categories overlapped, a miner could appear in more than one occupational group, and the analysis did not measure occupation-specific duration or individual dust exposure.

Continuous miner operators had an adjusted prevalence ratio of 1.8 for coal workers’ pneumoconiosis compared with miners who had never been continuous miner operators. The estimate had a 95% confidence interval of 1.6 to 2.0. For progressive massive fibrosis, their adjusted prevalence ratio was 3.0, with a 95% confidence interval of 2.3 to 4.0. Roof bolters also had elevated adjusted prevalence ratios: 1.4 for coal workers’ pneumoconiosis, with a 95% confidence interval of 1.3 to 1.6, and 1.4 for progressive massive fibrosis, with a 95% confidence interval of 1.1 to 1.9. In absolute numbers, 663 continuous miner operators and 770 roof bolters had pneumoconiosis, while 117 and 103, respectively, had progressive massive fibrosis.

Some other occupational groups had lower prevalence after adjustment for total underground tenure. The adjusted coal workers’ pneumoconiosis prevalence ratio was 0.9 for shuttle car operators, with a 95% confidence interval of 0.8 to 1.0; 0.7 for laborers, with a 95% confidence interval of 0.6 to 0.8; and 0.8 for belt, conveyor and belt-cleaning workers, with a 95% confidence interval of 0.7 to 0.9. Corresponding progressive massive fibrosis ratios were 0.9 for shuttle car operators, 0.6 for laborers and 0.5 for belt-related workers. These values should not be interpreted as protective effects of those jobs. The models compare broad lifetime occupational categories while adjusting only for total mining tenure, not the timing, duration or intensity of exposure within each job.

Central Appalachia, defined for the study as Kentucky, Virginia and West Virginia, accounted for 14,284 of the 30,319 miners. Coal workers’ pneumoconiosis was detected in 1,204 of them, a prevalence of 8.4%, compared with 243 of 16,035 miners elsewhere, or 1.5%. Progressive massive fibrosis occurred in 182 Central Appalachian miners, or 1.3%, compared with 13 miners elsewhere, or 0.1%. After adjustment for underground mining tenure, the regional prevalence ratio was 3.9 for coal workers’ pneumoconiosis, with a 95% confidence interval of 3.4 to 4.5, and 10.0 for progressive massive fibrosis, with a 95% confidence interval of 5.7 to 17.5. These are cross-sectional geographic contrasts rather than evidence of a change in prevalence over time.

The regional disparity was visible across occupational groups rather than being confined to the two jobs with the highest overall prevalence. Within Central Appalachia, tenure-adjusted coal workers’ pneumoconiosis prevalence ratios ranged from 3.3 for laborers, with a 95% confidence interval of 2.6 to 4.2, to 5.1 for continuous miner operators, with a 95% confidence interval of 4.1 to 6.3. Progressive massive fibrosis ratios ranged from 8.0 for continuous miner operators, with a 95% confidence interval of 4.2 to 15.3, to 19.1 for laborers, with a wide 95% confidence interval of 4.7 to 78.4. The number of cases was small in some comparisons, so estimates based on few outcomes had substantially greater uncertainty.

Underground mining tenure was associated with greater radiographic severity. Among the 1,447 miners classified as having coal workers’ pneumoconiosis, 921 had at least 25 years of underground mining experience. Of the 195 miners with progressive massive fibrosis, 149 were in that tenure group. Miners with pneumoconiosis had a median tenure of 28 years, compared with 16 years among miners without it, and their median age was 51 years rather than 43. Progressive massive fibrosis also appeared among miners with shorter tenures, including four cases among those with fewer than 10 years and 10 among those with 10 to 14 years. The observational analysis could not determine how such outcomes related to exposure intensity, individual disease progression or other factors.

The occupational pattern was consistent with earlier exposure measurements cited by the researchers, which found some of the highest respirable coal mine dust concentrations among continuous miner operators and roof bolters. Continuous mining can involve cutting coal and surrounding rock, while roof bolting can involve drilling into overhead rock and may generate respirable crystalline silica. Thin-seam conditions common in Central Appalachia can require more extensive cutting through surrounding strata. Previous pathology and radiographic investigations cited in the paper associated substantial silica and silicate burdens in miners’ lungs with severe or rapidly progressive disease. The present study, however, contained no quantitative individual dust-exposure data and therefore could not establish an exposure-response relationship or attribute risk to a single job.

The study has several limitations. Participation in the surveillance program was voluntary, so participants may not represent all US underground coal miners. Restriction to working miners could also introduce a healthy-worker survivor effect. Occupational histories were self-reported, workers frequently moved among jobs, and categories did not distinguish job-specific tenure or exposure intensity. Although the prevalence models adjusted for total underground tenure, residual confounding by age, sex and other factors remains possible. The analysis also included an observational sample of participants rather than a nationally representative random sample. Despite these constraints, its large sample, coverage of multiple US mining regions and standardized radiographic classifications show a persistent association between dusty mining work, mining tenure and the prevalence of radiographically detected occupational lung disease.

Subject of Research: Occupation- and region-specific prevalence of coal workers’ pneumoconiosis among 30,319 underground coal miners

Article Title: Assessment of pneumoconiosis by dusty job type among underground coal miners participating in the Coal Workers’ Health Surveillance Program,1991–2024

Article References: Myers, N. T., Blackley, D. J., Reynolds, L., Laney, A. S., & Hall, N. B. (2026). Assessment of pneumoconiosis by dusty job type among underground coal miners participating in the Coal Workers’ Health Surveillance Program,1991–2024. Frontiers in Public Health, 14, Article 1970741. https://doi.org/10.3389/fpubh.2026.1970741

Image Credits: AI Generated

DOI: 10.3389/fpubh.2026.1970741

Keywords: coal workers’ pneumoconiosis, progressive massive fibrosis, underground coal mining, respirable coal dust, crystalline silica, occupational exposure, Central Appalachia, radiographic surveillance, mining tenure, continuous miner operators, roof bolters, NIOSH

The patient reported seven days of fever, upper abdominal pain and bilateral lower-limb pain when he arrived at the medical ward. He also had yellow-red discoloration of the sclera, dark urine, pale stools and generalized itching. His history included a 10-pack-year smoking history and reported consumption of one or two alcoholic drinks per day for five to seven years, although he had been abstinent for five months and could not recall the type of beverage, serving size or alcohol concentration. He reported no biliary colic, known gallstones or use of hepatotoxic medicines. On admission, his blood pressure was 85/50 mmHg, pulse rate 90 beats per minute, respiratory rate 28 breaths per minute, oxygen saturation 95% on room air and temperature 98.8°F. Examination showed marked icterus and conjunctival suffusion without peripheral signs of chronic liver disease. His abdomen was soft and nontender, with no right-upper-quadrant tenderness, guarding or rigidity.

Although fever, jaundice and upper abdominal pain ordinarily prompt evaluation for acute cholangitis, the patient did not meet Charcot’s triad because abdominal tenderness was absent. Initial testing showed predominantly conjugated hyperbilirubinemia: total bilirubin was 10.6 mg/dL and the direct fraction was 9.81 mg/dL. Alkaline phosphatase was elevated at 267 U/L and gamma-glutamyl transferase at 105 U/L, whereas alanine aminotransferase was mildly increased at 58.4 U/L, creating a cholestatic biochemical pattern. The total leukocyte count was 13.8 × 10^3/μL, with 92.4% neutrophils, and the platelet count was markedly reduced to 20 × 10^3/μL. The erythrocyte sedimentation rate was 95 mm/h and C-reactive protein concentration was 223 mg/L, indicating a substantial systemic inflammatory response.

Renal function was severely compromised at presentation. Blood urea was 169 mg/dL, serum creatinine was 4.97 mg/dL and the patient had oliguria, indicating acute kidney injury. Urinalysis showed two-plus protein, pus cells, mild bacteria and granular casts. Prothrombin time was 15.4 seconds, activated partial thromboplastin time 46 seconds and the international normalized ratio 1.28. Screening was negative for hepatitis B surface antigen, anti-hepatitis C virus and HIV. Dengue NS1 antigen was negative, as were malaria immunochromatographic testing and malarial parasite smear. Blood culture was negative, although additional tests for typhoid fever were not performed. A chest radiograph showed clear lung fields without consolidation or pleural effusion.

Abdominal ultrasonography identified no hepatobiliary abnormality, and the common bile duct measured 0.4 cm without evidence of obstruction. This made acute cholangitis substantially less likely because cholangitis commonly arises in association with biliary obstruction, such as a common duct stone or neoplasm. The clinicians consequently considered a wider differential that included acute cholangitis, dengue, malaria, sepsis with multiorgan failure, viral hepatitis, drug-induced liver injury and other tropical febrile illnesses. Negative viral and malaria studies weakened several alternatives, while the lack of a relevant medication history made drug-induced liver injury less likely. The combination of cholestatic jaundice, acute kidney injury, thrombocytopenia and conjunctival suffusion instead favored severe leptospirosis. His work as a farmer, repeated exposure to wet fields and prominent calf muscle pain further supported that possibility.

Leptospirosis is a globally distributed bacterial zoonosis associated particularly with populations affected by socioeconomic vulnerability. Pathogenic Leptospira species infect animal hosts such as rodents, which can shed the organisms in urine. Human infection can follow occupational or recreational contact with contaminated water or soil, with entry through abraded skin or mucous membranes. Its early presentation is often nonspecific, with fever, headache and muscle pain that can resemble dengue, influenza, malaria and other acute febrile illnesses. Approximately 10% of patients develop severe disease. The source article describes a pathogenesis involving direct tissue injury, immune-mediated mechanisms, endothelial dysfunction, disturbed microcirculation and multiorgan damage. Severe manifestations include Weil’s syndrome, classically defined by conjunctival suffusion, jaundice and acute kidney injury, as well as pulmonary, hepatic, renal, cardiac, hematological and gastrointestinal abnormalities.

A serum anti-leptospiral IgM enzyme-linked immunosorbent assay produced an index value of 2.18, above the assay’s positive threshold of 1.1. The result was considered consistent with acute leptospirosis when interpreted alongside the clinical and laboratory pattern. Confirmatory polymerase chain reaction testing for Leptospira DNA and microscopic agglutination testing were unavailable at the treating center. IgM ELISA therefore served as supportive rather than definitive confirmation in this case; the report notes that the method can cross-react and must be interpreted in an appropriate clinical context. Creatine phosphokinase activity was 39 U/L, within the laboratory’s stated reference range of 39–308 U/L.

Because the patient had severe jaundice and renal dysfunction and both leptospirosis and acute cholangitis remained under consideration, the medical team began empirical intravenous ceftriaxone twice daily with intravenous normal saline for hydration. Ceftriaxone was selected because it covers common biliary pathogens and is also an established first-line parenteral agent for severe leptospirosis. Penicillin G and doxycycline are also used for milder disease, whereas third-generation cephalosporins are preferred for severe disease with multiorgan involvement in the case report. Intravenous paracetamol was prescribed as needed for fever and pain, although the patient experienced only one episode of fever during the four-day hospital stay. He received four days of intravenous ceftriaxone in hospital and was advised to complete three additional days at a local outpatient facility, for seven days in total.

Serial laboratory measurements showed changes consistent with improvement after treatment began, although the renal trajectory was not uniformly downward on every measure. By hospital day three, the leukocyte count had fallen to 10.9 × 10^3/μL, the neutrophil percentage to 73% and total bilirubin to 6 mg/dL. Platelet count rose from 20 × 10^3/μL at admission to 22 × 10^3/μL on day one, 31 × 10^3/μL on day two and 55 × 10^3/μL on day three. Alkaline phosphatase declined from 267 U/L at admission to 250, 202 and 202 U/L on successive days. Blood urea initially rose from 169 mg/dL at admission to 196 mg/dL on day one, then fell to 162 mg/dL on day two and 85 mg/dL on day three. Serum creatinine declined across the same interval, from 4.97 to 4.5, 3.6 and 2 mg/dL. The patient remained hemodynamically stable and developed no bleeding despite severe thrombocytopenia, so platelets, fresh frozen plasma and cryoprecipitate were not given; the low platelet count was managed conservatively with close monitoring.

At follow-up one week after the antibiotic course ended, the patient reported complete resolution of fever, jaundice, abdominal pain and calf myalgia. Repeat laboratory testing showed near-normalization of bilirubin, renal parameters, leukocyte count and platelet count. Long-term follow-up was unavailable, so the report cannot establish whether renal recovery was sustained or whether chronic complications later emerged. Severe leptospirosis can produce acute kidney injury through tubulointerstitial damage, often alongside jaundice, thrombocytopenia and abnormal urine findings. Other described severe forms include pulmonary hemorrhagic syndrome, acute respiratory distress syndrome and manifestations that can meet criteria for sepsis because of intense systemic inflammation and multiorgan failure. In this patient, the combination of jaundice, acute kidney injury and hematological abnormalities corresponded to the reported pattern of Weil’s syndrome.

The central diagnostic lesson is that a cholestatic liver profile alone does not establish acute cholangitis. Although the patient had fever, upper abdominal pain, jaundice, leukocytosis and sharply elevated inflammatory markers, imaging showed no biliary obstruction, the abdominal examination did not reproduce the pain and blood cultures were negative. Severe kidney injury, thrombocytopenia, conjunctival suffusion, calf myalgia and exposure to wet agricultural fields instead formed a more coherent pattern of leptospirosis. The report supports considering the infection among the causes of suspected cholangitis when no obstruction is demonstrated, particularly in endemic settings and among people with compatible occupational exposure. As a single case without a comparator group and with limited long-term follow-up, it cannot establish comparative treatment effectiveness or population-level outcomes. Its value instead lies in documenting a severe, non-obstructive presentation and the clinical and laboratory pattern that allowed the diagnosis to be reconsidered.

Subject of Research: Severe leptospirosis presenting as Weil’s syndrome with cholestatic jaundice and multiorgan dysfunction that mimicked acute cholangitis.

Article Title: Weil's Syndrome Masquerading as Acute Cholangitis: A Case Report of a Farmer With Leptospirosis

Article References: Shaikh, A. A., Shaikh, F., Arshad, S., Devrajani, T., Ahmed, H., & Al‐Dhaheri, M. (2026). Weil's Syndrome Masquerading as Acute Cholangitis: A Case Report of a Farmer With Leptospirosis. Clinical Case Reports, 14(10), Article e73751. https://doi.org/10.1002/ccr3.73751

Image Credits: AI Generated

DOI: 10.1002/ccr3.73751

Keywords: leptospirosis, Weil’s syndrome, acute cholangitis, cholestatic jaundice, acute kidney injury, case report, thrombocytopenia, occupational exposure, bacterial zoonosis, conjugate hyperbilirubinemia, Weil's, Syndrome

The study assessed serum concentrations of seven PFAS in Korean firefighters and the general population to characterize exposure levels, compositional profiles, and relationships with demographic, occupational and lifestyle factors. Principal component analysis showed substantial overlap between the groups, indicating that the analysis did not cleanly separate them. Within that overlap, PFOA and selected long-chain perfluoroalkyl carboxylic acids contributed more strongly to variability among firefighters. The results therefore support a difference in the typical PFOA concentration and the mixture of compounds detected, rather than a complete separation between the groups. The available study summary does not report individual distributions, sample sizes or clinical outcomes.

Length of service was positively correlated with several PFAS in unadjusted analyses of firefighters. In the primary multivariable analyses, positive associations remained for perfluorononanoic acid (PFNA) and PFHxS after accounting for the study’s selected demographic, occupational and lifestyle variables. Those associations were attenuated in sensitivity analyses that used alternative covariate specifications, making their stability less certain. In the general population, selected relationships involving age, height, and time spent walking or strolling persisted after adjustment. These statistical associations do not establish that occupational tenure or the other measured factors caused the observed serum concentrations, and the summary reports no causal analysis.

The findings are limited to the populations, compounds and variables included in the study. They characterize measured serum exposure rather than demonstrating that any individual firefighter had elevated exposure, and they do not establish when exposure occurred or whether concentrations changed over a career. No health effects were evaluated in the reported results. The authors nevertheless concluded that the contrast between the groups, together with the occupational and other correlates identified within them, underscores the importance of considering occupational characteristics when assessing and managing PFAS exposure.

Subject of Research: Serum PFAS exposure and associated factors in Korean firefighters

Article Title: Assessment of per- and polyfluoroalkyl substances (PFAS) exposure in Korean firefighters by serum analysis

Article References: Choi, S., & Oh, J.-E. (2026). Assessment of per- and polyfluoroalkyl substances (PFAS) exposure in Korean firefighters by serum analysis. Environmental Geochemistry and Health, 48(16), Article 647. https://doi.org/10.1007/s10653-026-03547-4

Image Credits: AI Generated

DOI: 10.1007/s10653-026-03547-4

Keywords: PFAS, PFOA, firefighters, serum analysis, South Korea, occupational exposure, PFOS, PFHxS, PFNA, environmental health, Assessment, per-

The review, conducted by a team of researchers at Huazhong University of Science and Technology in Wuhan, China, followed the PRISMA guidelines for systematic reviews and searched the SCOPUS database across multiple stages between April and October 2025. After an exhaustive screening process that began with more than 400 identified records and expanded through successive keyword searches covering waste classification, disposal, recycling, health issues, and health protection, the team ultimately coded 81 peer-reviewed articles for detailed analysis. The quality of the reviewed studies ranged from moderate to high, with 68 percent published in journals carrying an Impact Factor or Citescore, and a bias assessment of a randomly selected subset confirmed that study quality was broadly consistent with publication venue standards.

The central finding is striking in its breadth: AI technologies are now deployed across all five major stages of waste management, from source classification and separation through collection logistics, treatment and resource utilization, final disposal, and even strategic planning. The classification and separation stage dominates the literature, accounting for 47.5 percent of reviewed articles, with source-level classification and management alone making up 29.2 percent. Computer vision systems, smart trash bins, and sensor-equipped recycling plants can identify and sort waste in real time, while AI tools at the point of waste generation monitor disposal behavior and detect misclassification before hazardous items ever reach a conveyor belt.

Underneath these applications lies a taxonomy of four technical paradigms. Supervised learning, which learns mappings between input and output variables from historical data, appears in 39.5 percent of articles, powering convolutional neural networks like YOLO, ResNet, and VGG variants that achieve high-precision waste identification, as well as models such as XGBoost and random forest that predict municipal waste generation trends. Deep learning is the largest single category at 51.9 percent, encompassing hybrid CNN-LSTM architectures that simultaneously classify waste images and forecast gas production, transformer-based models, and lightweight networks designed for high-speed sorting at container terminals. By contrast, unsupervised learning techniques such as K-means clustering and self-organizing maps appear in only 4.9 percent of studies, and reinforcement learning in just 2.4 percent, mainly optimizing catalytic degradation of plastics through adaptive trial-and-error reward mechanisms.

When the authors coded the health risks these technologies address, five distinct categories emerged: chemical toxicity risk at 27.2 percent, general public health risk at 21 percent, infectious risk at 9.9 percent, physical injury risk at 3.7 percent, and occupational exposure risk, the largest category, at 42 percent. Crucially, more than 40 percent of the reviewed articles focus on how AI mitigates risks tied to occupational exposure, and the affected populations extend well beyond formal employees. Informal recyclers sorting e-waste without protective equipment, demolition workers, healthcare workers handling biomedical waste, and residents of surrounding communities all appear as beneficiaries in the reviewed literature, though the authors note that health outcomes are generally inferred from empirical study designs rather than directly assessed through medical measurement.

The review identifies three primary pathways through which AI actually alleviates hazards. The first is automated risk-source isolation: image recognition systems can detect infectious medical waste, electronic components containing hazardous chemicals, or damaged chemical containers and sort them out of the stream before any human touches them, eliminating the direct contact that defines traditional manual sorting. The second is robotic substitution for high-risk tasks. AI-driven robotic arms and automated production lines now perform repetitive, high-exposure operations such as sorting, crushing, and transporting waste, shielding workers from physical cuts, biological infections, and dust inhalation while relocating them to back-end monitoring and management roles.

The third pathway operates at the macro level, combining real-time environmental monitoring with predictive analytics. Sensor networks deployed at landfills and processing facilities continuously track air quality, toxic gas concentrations, and leachate leakage, and supervised and deep learning models can issue early warnings when conditions turn dangerous, allowing managers to evacuate personnel or adjust operations before sudden, high-concentration exposures occur. Unsupervised learning adds another layer by mining long-term datasets of environmental records, worker health profiles, and operational logs to uncover latent risk patterns and chronic-disease hotspots. Cluster analysis and pollution dispersion simulations can then delineate zones with differentiated risk levels, providing a scientific basis for tiered protection standards, optimized facility layouts, and rationally arranged working hours.

Yet the authors are emphatic that technology alone cannot deliver these gains. Their policy analysis identifies four institutional priorities for responsible AI deployment. Data privacy frameworks and unified technical standards for waste classification must accompany the large-scale data collection carried out by smart bins and sensor networks. High-risk waste streams need targeted regulation, such as legally mandated extended producer responsibility for e-waste and machine learning-optimized catalytic degradation for plastics. Incentive structures like tax breaks, subsidies, and green procurement should be paired with accountability mechanisms, including cross-regional enforcement against illegal dumping supported by remote sensing and image recognition. Perhaps most urgent is the question of equity: the review stresses integrating the informal recycling sector into formal systems, with governments funding local-language digital literacy and AI operation training so that waste pickers can transition into AI sorting oversight, waste inspection, and emission monitoring roles rather than being displaced by automation.

At the industry level, the review calls for shifting from efficiency-dominated design to health-oriented system development, scaling up demonstration projects for AI-integrated sorting and real-time risk monitoring in the highest-risk settings such as landfills, sorting facilities, and informal recycling zones, and strengthening collaboration between research institutions, waste enterprises, and public health authorities. It also ties these efforts to the circular economy: a United Nations Environment Programme report cited in the study projects annual net gains of 108.5 billion dollars from circular economy approaches, and AI-enabled waste characterization, demand forecasting, and material flow tracking could improve the stability and quality of recycled resources while enhancing EPR accountability.

The study is candid about its limitations. It does not systematically distinguish mature technologies from conceptual prototypes, many reviewed articles do not report measurable outcomes, and grey literature such as preprints and policy documents was excluded. It also flags an understudied irony: AI devices themselves generate e-waste, energy consumption, and noise pollution. Still, the core message stands out as a genuine reframing. AI in waste management, the authors argue, is not merely a technical achievement but a socio-technical transformation that integrates efficiency, health, and equity, and public health researchers should borrow medical research methodologies to quantify exactly how many exposures, infections, and injuries technological innovation is preventing. Without supportive institutions, they warn, even the most advanced algorithms cannot achieve safe, scalable, and equitable deployment, and the workers most exposed to waste hazards risk being left behind by the very technologies designed to protect them.

Subject of Research: Artificial intelligence applications for occupational and environmental health risk mitigation in waste management

Article Title: Deploying artificial intelligence for occupational and environmental health in waste management: a systematic review

Article References: Li, W., Ge, Z., Wang, H., Yuan, M., & Yin, Z. (2026). Deploying artificial intelligence for occupational and environmental health in waste management: a systematic review. International Journal of Public Health, 71, Article 1610020. https://doi.org/10.3389/ijph.2026.1610020

Image Credits: AI Generated

DOI: 10.3389/ijph.2026.1610020

Keywords: artificial intelligence, waste management, occupational health, environmental health, systematic review, deep learning, machine learning, robotics, public health, circular economy, occupational exposure, informal waste sector

That gap is what motivated a team of Swedish occupational and environmental medicine researchers to carry out one of the most comprehensive surveys of isocyanic acid ever attempted. Writing in Environmental Science and Pollution Research, Gunilla Runström Eden of Sahlgrenska University Hospital and the University of Gothenburg, together with colleagues in Gothenburg and Örebro, collected 173 air samples across 16 different occupational and environmental settings between June 2020 and September 2021. The study was designed to compare relative concentrations across a wide range of environments rather than to conduct a traditional exposure assessment in a few select workplaces, and the results were benchmarked against the only occupational exposure limit for isocyanic acid in the world, the Swedish limit of 18 micrograms per cubic metre as an 8-hour mean and 36 micrograms per cubic metre over a 5-minute period.

The analytical approach relied on derivatisation during sampling with di-n-butylamine, followed by liquid chromatography mass spectrometry. Most measurements used the Supelco Easysampler denuder, while impingers with a higher flowrate of 1 litre per minute were deployed for very short tasks and for cigarette smoke measurements, where the higher flow better mimicked the act of smoking. Two samplers were coupled in series to catch possible breakthrough, field blanks were collected and used to correct the results, and all airflows were set and checked with digital flow meters before, during and after sampling. The detection limit was 0.006 micrograms per sample and the quantification limit 0.020 micrograms per sample. Personal samplers were placed in the breathing zone of workers wherever the COVID-19 pandemic allowed, but in many workplaces only stationary measurements were possible, with samplers placed within a metre of hypothesised sources in the newly investigated environments.

The highest concentrations were consistently found in industries using urea-based binders at elevated temperatures. At a company producing wooden laminate products, average personal exposure reached 48 micrograms per cubic metre with a maximum of 92 on the first measurement occasion, and repeated measurements in June were lower but still relatively high against the exposure limit, averaging 19 with a maximum of 30. Some stationary measurements were extreme, with the highest exceeding 264 micrograms per cubic metre. At a second building-material company, personal measurements characterised as a worst-case scenario averaged 2 micrograms per cubic metre with a maximum of 30. The team notes that these levels are in the same magnitude as reported 10 to 20 years ago in similar environments, with earlier studies ranging from below 4 up to 573 micrograms per cubic metre, suggesting little has changed in terms of exposure in this sector.

One of the most striking findings concerned mineral wool insulation during its initial heating phase. Glass wool and mineral wool are manufactured with binders containing urea, and Sweden’s large combined heat and power plants use these materials on a massive scale. At a brand-new facility, measurements taken over time as running-in temperatures increased showed emissions rising to a maximum of 62 micrograms per cubic metre, remaining elevated for a long period after start-up. The highest levels occurred at the first temperature rise above 200 degrees Celsius, consistent with earlier observations that isocyanic acid emission begins at 133 degrees, the point where urea starts to melt. With repeated temperature rises, levels stayed high but far below those measured during the first warming. During minor renovation of already insulated heating parts, by contrast, no detectable levels were found. The operations were aware of the risks and imposed personal protective equipment during start-up phases.

Thermal processing of polyurethane produced lower but spatially widespread concentrations. At a very large company with several hundred employees, a hot process involving polyurethane products sat centrally in a production hall of roughly 20,000 square metres. Close to the emission process, both diisocyanates and monoisocyanates could be detected, but further away only isocyanic acid remained detectable, indicating that it is not very reactive and can persist far from its source, in line with an estimated residence time of 8 hours in air. Concentrations were found throughout the building, though levels stayed below the Swedish exposure limit, with average personal exposure of 3 micrograms per cubic metre and a maximum of 5.

In sharp contrast, the newly investigated environments showed generally low or negligible levels. Across five restaurants, three food industries, linoleum welding, diathermy procedures, asphalt work and lawn mowing, concentrations were well below the exposure limit or below detection limits. Only one restaurant, where hamburgers were fried, generated concentrations above the detection limit, with a maximum of 0.6 micrograms per cubic metre, and the team suggests that poorer ventilation there and in home frying environments may have contributed. During linoleum mat welding at 300 to 350 degrees Celsius, a measurement directly in the formed smoke showed 6 micrograms per cubic metre, but personal and background samples detected nothing. At a dermatology clinic, isocyanic acid was detected during CO2 laser use at around 1 microgram per cubic metre but not during diathermy, a likely consequence of the temperature difference between the two techniques, roughly 400 degrees for the laser against about 100 for diathermy. Asphalt workers showed detectable but very low exposure with a maximum of 0.5 micrograms per cubic metre, and mowing a lawn with a petrol mower produced exposure just above 1 microgram per cubic metre. In 3D printing with thermoplastic polyurethane filament, emissions were confirmed inside one printer hood but not outside it, and a third printer and filament combination showed nothing at all.

The environmental measurements fill a significant European data gap. Outdoor air in Gothenburg, sampled at three locations with different traffic intensities over 20-hour periods, showed uniformly low concentrations between 0.14 and 0.25 micrograms per cubic metre, with a mean of 0.12, in the lower range of previously reported outdoor data and below recent measurements from China of around 0.7. Diesel engine exhaust sampled directly from exhaust pipes in an experimental setup ranged between 0.5 and 4.6 micrograms per cubic metre, with no clear pattern across engines, fuels or driving cycles, and the addition of urea-containing diesel exhaust fluid such as AdBlue did not generally raise emissions. The team concludes that internal combustion engines are an important source of the isocyanic acid found in urban air.

Cigarette smoke, however, stands in a category of its own. Direct measurements in cigarette smoke confirmed extremely high isocyanic acid levels of up to 4300 micrograms per cubic metre, while side-stream exposure measured at 1 to 5 micrograms per cubic metre was considerably lower. The smoke also contained extremely high levels of methyl isocyanate, over 6000 micrograms per cubic metre, findings consistent with literature dating back to 1965 and replicated in a larger 2025 study by the same group. The team notes that smoking a single cigarette provides an exposure above the Swedish 8-hour limit, making smoking one of the most significant personal exposures to this compound that most people will ever encounter.

The health implications remain the great unresolved question. Isocyanic acid is biochemically active, participating in a protein modification called carbamylation, and the isocyanate family is well known for causing asthma and other respiratory effects. Only one occupational study of monoisocyanate health effects has been identified, finding nasal symptoms and a small reduction in forced expiratory volume, and a more recent report described three workers exposed to decomposition products during hot iron cauterisation, with personal isocyanic acid measurements between 331 and 435 micrograms per cubic metre, two of whom had asthma, though the link to isocyanic acid is unclear. The Swedish limit itself is based on similarity to methyl isocyanate rather than on direct health data. The survey shows that higher isocyanic acid concentrations are mainly associated with industrial high-temperature handling of urea or polyurethane-based materials and with cigarette smoke, while everyone can expect exposure of around 0.2 micrograms per cubic metre outdoors and slightly higher indoors. The researchers caution that some environments were surveyed only once and that sampling times varied, so results should be used to rank environments rather than to determine whether limits were exceeded. A follow-up exposure assessment in select environments is planned, and the team stresses that better health effects data are urgently needed to understand what these exposures truly mean.

Subject of Research: Environmental Science and Pollution Research

Article Title: Isocyanic acid measurements in Swedish industries and environments

Article References: Eden, G. R., Storsjö, T., Johansson, A., Andersson, L., & Tinnerberg, H. (2026). Isocyanic acid measurements in Swedish industries and environments. Environmental Science and Pollution Research. https://doi.org/10.1007/s11356-026-38302-w

Image Credits: AI Generated

DOI: 10.1007/s11356-026-38302-w

Keywords: isocyanic acid, occupational exposure, air quality, industrial emissions, polyurethane, urea binders, cigarette smoke, Sweden, Isocyanic, acid, measurements, Swedish

The team, registered with PROSPERO and reported according to the PRIOR guidelines for overviews of reviews, searched four major databases, PubMed, Embase, Scopus, and Web of Science, for studies published up to October 15, 2024, with no restrictions on language, geography, or publication date. From 643 identified records, the reviewers screened 290 by title and abstract and ultimately included nine systematic reviews. Eight of these combined cohort and case-control studies, while one relied solely on cohort data. Ovarian cancer dominated the literature, appearing in five of the nine reviews, all focused on cosmetic talc use. The remaining reviews examined occupational exposure in relation to mesothelioma, stomach cancer, and a broad range of other malignancies. Cosmetic exposure was the most frequently studied route, appearing in six of the nine reviews.

A distinctive strength of this umbrella review is its methodological scrutiny. Using the AMSTAR-2 tool, which grades systematic reviews from high to critically low confidence across sixteen domains, the authors found sobering results: only one review earned a moderate confidence rating, while seven were judged to be of critically low confidence. The most common failings were the absence of registered protocols, failure to report reasons for excluding studies, and incomplete assessment of risk of bias in the underlying primary studies. The team also performed an overlap analysis, quantifying how much the included reviews reused the same primary studies. The corrected overlap was 9.2 percent, classified as moderate, driven largely by one comprehensive review that absorbed a large share of the available literature. This redundancy means the apparent consistency of findings across reviews may partly reflect dependence on a shared pool of evidence rather than genuine replication.

On the central question of cosmetic talc and ovarian cancer, four of the five relevant reviews reported statistically significant associations. One review included in the synthesis reported a hazard ratio of 2.13 (95 percent confidence interval 1.54 to 2.94) in one of two studies it examined, while no added risk was found for cervical or uterine cancer. The broader literature paints a consistent but troublingly design-dependent picture. Meta-analyses dominated by case-control studies have reported odds ratios around 1.31, rising to approximately 1.42 at high cumulative exposures of more than 3,600 applications. Yet when the analysis is restricted to prospective cohort studies, the association largely evaporates, with one pooled estimate of relative risk 1.02 (95 percent CI 0.85 to 1.20) showing no significant elevation. The signal that does appear is concentrated in serous carcinoma, the most common histological subtype of ovarian cancer.

This discrepancy between retrospective and prospective designs is the crux of the causal debate. Case-control studies ask women who already have cancer to recall hygiene practices from decades earlier, a setup notoriously vulnerable to recall bias, particularly when the suspected risk factor has been widely publicized in the media and in litigation. Differential misclassification of exposure can inflate apparent associations. Comprehensive reviews that integrated multiple lines of epidemiological evidence have concluded that the consistent findings may be shaped by these methodological biases and residual confounding rather than by a direct biological effect, and that the evidence is insufficient to support a causal relationship between talc exposure and cancer in humans.

The proposed biological mechanism remains equally unresolved. The leading hypothesis holds that talc particles applied to the perineum can migrate upward through the genital tract to reach the ovaries, where they provoke chronic inflammation. Inflammation is a well-established contributor to carcinogenesis: inflammatory cells release cytokines and reactive oxygen species that damage DNA and stimulate cell proliferation. Animal and human tissue studies have suggested talc particles may promote proliferation, but direct evidence demonstrating particle migration to ovarian tissue in humans remains limited. Notably, a meta-analysis of women using talc-dusted contraceptive diaphragms, a route that bypasses the perineal migration pathway, found no conclusive evidence of risk, with a relative risk of 1.03 (95 percent CI 0.80 to 1.37). Reviews weighing epidemiological, mechanistic, and experimental evidence together have classified the data as suggestive of no association between talc applied to the female genitalia and cancers of the female reproductive system at human-relevant exposure levels.

The occupational picture is murkier still. One meta-analysis of occupational cohorts found a statistically significant association between talc exposure and stomach cancer (relative risk 1.21; 95 percent CI 1.03 to 1.42), and an elevated risk of colorectal cancer was also reported (standardized incidence rate ratio 1.59; 95 percent CI 1.07 to 2.26). No significant associations emerged for pleural, peritoneal, lung, bladder, kidney, or prostate cancers. But the gastric cancer finding carries a critical caveat: when the analysis was restricted to talc products free of asbestiform fibers, the association lost statistical significance (relative risk 1.26; 95 percent CI 0.97 to 1.63). Historical talc deposits were sometimes contaminated with asbestos, and most occupational cohorts were assembled decades ago with little characterization of actual exposure levels or co-exposures such as asbestos, silica, or smoking. Residual confounding from asbestos contamination therefore cannot be excluded, making the occupational evidence suggestive rather than conclusive.

Complicating matters further, the International Agency for Research on Cancer recently classified talc not containing asbestos as probably carcinogenic to humans, a Group 2A designation. That decision has itself become controversial. A critical review argued that the reclassification stemmed primarily from changes in the evaluation framework rather than from new epidemiological or laboratory evidence, and highlighted persistent uncertainty over mineralogical characterization and the interpretation of mechanistic data. The distinction matters enormously, because talc is ubiquitous: it appears in cosmetics, pharmaceuticals, food additives in some countries, paper, plastics, ceramics, paints, and rubber. Yet the systematic reviews included in this umbrella focused almost exclusively on perineal cosmetic use and occupational exposure, leaving the vast majority of alternative exposure pathways unexamined. The findings should therefore not be read as a verdict on talc exposure in general.

Context also matters for interpreting the size of any risk. Even under a causal hypothesis, the relative risk estimates of roughly 1.2 to 1.3 for perineal talc use are smaller than those associated with genetic, hormonal, or metabolic determinants of ovarian cancer, suggesting the population-level contribution of talc would be modest. The most recent comprehensive review could identify only a single prospective study showing a statistically significant relationship, too few to generate a pooled estimate. Dose-response evidence is limited, biological plausibility is unconfirmed in humans, and the umbrella review’s authors acknowledge their own design limitations, including dependence on the quality of prior reviews, heterogeneous exposure classifications, and the inability to perform second-order meta-analyses because of study overlap.

The bottom line is neither exoneration nor condemnation. The umbrella review confirms that a small to moderate statistical association between cosmetic talc use and ovarian cancer appears repeatedly in the literature, but that this association rests overwhelmingly on retrospective studies of critically low methodological confidence, with prospective evidence thin and inconsistent. For occupational exposures, the gastrointestinal cancer signals are entangled with possible asbestos contamination that modern studies have yet to disentangle. The authors call for future prospective studies incorporating rigorous mineralogical characterization of talc, standardized assessment of co-exposures, and proper control of confounding variables, alongside methodologically stringent systematic reviews. Until such work arrives, the talc-cancer question, one of the most contested in environmental health, remains open, and the scientific record urges caution on both sides of the debate.

Subject of Research: Association between talc exposure and cancer risk assessed through an umbrella review of systematic reviews and meta-analyses

Article Title: Talc Use and Risk of Cancer: An Umbrella Review and Overlapped Analysis

Article References: Mayta‐Tovalino, F., Cabanillas‐Lazo, M., Quispe‐Vicuña, C., Espinoza‐Carhuancho, F., & Hernandez, A. V. (2026). Talc Use and Risk of Cancer: An Umbrella Review and Overlapped Analysis. Cancer Reports, 9(10), Article e70705. https://doi.org/10.1002/cnr2.70705

Image Credits: AI Generated

DOI: 10.1002/cnr2.70705

Keywords: talc, talcum powder, ovarian cancer, umbrella review, systematic review, AMSTAR-2, carcinogenicity, occupational exposure, cosmetic talc, IARC, asbestos contamination, cancer risk

The research team, led by Sofia Eirini Chatoutsidou of the Technical University of Crete together with colleagues from the N.C.S.R. Demokritos research center and the National and Kapodistrian University of Athens, built their simulation around a realistic exposure pattern. They assumed eight hours per day of breathing diluted diesel exhaust, chosen to approximate an occupational setting such as a depot, loading dock, or roadside workplace, followed by sixteen hours of ordinary urban air pollution. That split matters because the two aerosols differ sharply in character. Diesel exhaust particles are soot agglomerates roughly 70 to 80 nanometers across, studded with polycyclic aromatic hydrocarbons, semi-volatile organics, and metals, while urban particles are fewer in number and spread across a broader size range.

The particle data came from measurements in Toronto, where urban air was sampled at a central intersection of two high-traffic roads, and from a heavy-duty diesel engine run at low load and intermediate speed, conditions that mimic urban cruising. Using a Scanning Mobility Particle Sizer, the diesel exhaust showed a number concentration of about 5.37 × 10⁴ particles per cubic centimeter, peaking near 70 to 80 nanometers, while urban air carried roughly 1.76 × 10⁴ particles per cubic centimeter. The authors checked these values against the wider literature and found them plausible: vehicles without diesel particulate filters can emit particles in the range of 10⁶ to 10⁷ per cubic centimeter, whereas filter-equipped vehicles drop to around 10⁴, though active filter regeneration events can spike concentrations back up by orders of magnitude.

To track where those particles go, the team used ExDoM2, a dosimetry model built on the semi-empirical respiratory tract framework of the International Commission on Radiological Protection. The model divides the human respiratory tract into five regions: the anterior nose, the posterior nasal passages with pharynx and larynx, the bronchial region, the bronchiolar region, and the deep alveolar-interstitial zone where gas exchange happens. Each region acts as a series of filters, and deposition in each depends on particle size, breathing rate, and the balance between aerodynamic mechanisms like impaction and settling and thermodynamic mechanisms like diffusion. For nanoparticles, diffusion dominates, which is precisely why particles smaller than 100 nanometers penetrate so effectively into the lung’s deepest recesses.

The headline result of the deposition simulations is stark. For an adult male of normal weight engaged in light exercise such as walking, 69 percent of inhaled nanoparticles from either diesel exhaust or urban air deposited in the alveolar-interstitial region, and combining that with the tracheobronchial zone means 86 percent of the inhaled nanoparticles ended up in the lungs after a single day. In absolute terms, one hour of diesel exposure delivered about 2.7 × 10¹⁰ particles to the lungs, corresponding to a surface dose of 4.15 × 10¹⁴ square nanometers and a mass dose of 9.9 micrograms. Surface area, rather than mass, turns out to be the critical metric, because rodent toxicology studies have shown that the tumor response to poorly soluble particles tracks the accumulated particle surface in lung tissue.

Clearance told an equally important story. During an eight-hour diesel exposure, 19.3 micrograms deposited in the extrathoracic region and 79.2 micrograms in the lungs, but after clearance only 9.4 and 71.6 micrograms respectively remained. That means the upper airways shed just over half of their deposited load, while the lungs cleared a mere 9.5 percent. Meanwhile, small fractions of the dose migrated elsewhere: 10.5 micrograms traveled to the esophagus, 5.9 micrograms were absorbed into the blood, and a trace amount reached the lymph nodes. The deep lung, with its slow macrophage-mediated clearance, effectively becomes a reservoir for diesel soot, and it is exactly this retained burden that the model projects forward over years.

When the simulations were extended to long-term exposure, the retained lung mass followed an exponential curve that reached a plateau after roughly 1,000 days, or about three years of constant exposure. Projected out to 10,000 days, approximately 27 years, the retained dose stabilized at around 7,786 micrograms for combined diesel and urban exposure, compared with 7,761 micrograms for diesel alone, a difference so small it underscores how overwhelmingly the eight-hour diesel window dominates the total burden. The saturated dose was roughly 77 times the initial one-day dose. The authors caution that this plateau reflects the assumption of unchanging exposure conditions; in reality, shifts in concentration or episodes of very high exposure can overwhelm alveolar macrophages, the lung’s first-line scavenger cells, and change the deposition picture entirely.

The most innovative step came next. Using the allometric scaling approach recommended by the Environmental Protection Agency, in which toxicity doses between species scale with body mass to the power of three-quarters, the team converted the long-term retained human lung dose into an animal equivalent dose. Because the target tissue is the lung itself, the scaling used lung masses rather than body masses: about 1,000 grams for a human lung versus 1.5 grams for a rat lung, a ratio of roughly 667. Smaller animals have higher metabolic rates and correspondingly higher dose accumulation, so the equivalent rat dose came out higher than the human dose. The converted values fell in the lower range of the experimental dose-response curve compiled from classic rat inhalation studies by Oberdörster, Miller, and others, where the logistic fit predicts a lung tumor proportion of 2.42 percent, with a 95 percent confidence interval of 0.073 to 6.12 percent.

Notably, this tumor estimate was essentially identical across all the receptor types the model examined, including normal-weight and overweight men and women at different activity levels. Variations in inhalation rate and body composition did shift the deposited dose, with males under light exercise receiving the highest doses among normal-weight individuals, while overweight females sitting at the same activity level received higher doses than their normal-weight counterparts. But once those doses were scaled to the rat equivalent, they all landed in the flat lower portion of the logistic curve, where the predicted tumor proportion barely changes. The implication is that, within the physiological variation explored here, exposure conditions, not personal characteristics, are the dominant driver of the modeled carcinogenic risk.

The study has clear limitations that the authors acknowledge. It relied on a single particle size distribution for all simulations, whereas real-world exposure varies constantly; it assumed fixed receptor characteristics and constant exposure conditions; and the allometric and clearance formulations carry their own uncertainties, as does fitting a logistic curve to a limited set of in vivo observations. Still, the work represents a meaningful bridge between two worlds that rarely speak directly: computational dosimetry of human inhalation and experimental rodent carcinogenicity. By quantifying exactly how much diesel soot accumulates in human lungs over a working lifetime and showing that the scaled equivalent sits within the tumor-producing range observed in rats, the study gives risk assessors a concrete, mechanistically grounded link between everyday traffic pollution and the cancer endpoint that regulators care about most. For the millions of workers who spend their shifts beside idling diesel engines, the message is hard to ignore.

Subject of Research: Respiratory tract dosimetry of diesel exhaust particles and its allometric link to lung tumor responses in rats

Article Title: Linking human respiratory tract dose from diesel exhaust particles to lung tumor responses observed in rats

Article References: Chatoutsidou, S. E., Chalvatzaki, E., Mammi-Galani, E., Diapouli, L., Gini, M. I., Manousakas, M. I., Kasdagli, M.-I., Samoli, E., Katsouyanni, K., Eleftheriadis, K., & Lazaridis, M. (2026). Linking human respiratory tract dose from diesel exhaust particles to lung tumor responses observed in rats. Air Quality, Atmosphere & Health, 19(10), Article 226. https://doi.org/10.1007/s11869-026-02115-0

Image Credits: AI Generated

DOI: 10.1007/s11869-026-02115-0

Keywords: diesel exhaust particles, lung dosimetry, nanoparticles, allometric scaling, lung cancer, air pollution, respiratory tract, clearance, occupational exposure, risk assessment, ExDoM2 model, rat toxicology

Mucormycosis is caused by environmental molds belonging to the order Mucorales, most notoriously the genus Rhizopus, whose spores float freely in soil, decaying organic matter, and damp air. In most people, inhaled spores are simply engulfed and destroyed by neutrophils and macrophages, the innate immune cells that patrol the airways. But when those defenses falter, as in diabetes, cancer, or organ transplantation, the spores germinate into broad, ribbon-like fungal hyphae that invade blood vessels with terrifying speed. This angioinvasion triggers thrombosis and tissue death, driving a fulminant infection that kills 40 to 50 percent of affected patients even with treatment. Diabetes remains the most common predisposing factor, associated with an overall mortality of roughly 46 percent, and more than half of all mucormycosis cases in large reviews occur in people with overt immunosuppression.

The Iranian patient’s initial symptoms were strikingly atypical, which is precisely why the diagnosis proved so treacherous. He complained of severe right-sided epigastric pain and excessive watering of the right eye, with no nasal congestion, no fever, and no neurological signs. His doctor prescribed topical ketorolac eye drops for presumed conjunctivitis. Instead of improving, he deteriorated: marked redness around the eye progressed to bruising-like ecchymosis and swelling, prompting admission to Prophet Azam Hospital at Kerman University of Medical Sciences. The authors of the report suggest that the abdominal pain may have reflected inadvertent ingestion of fungal spores, since gastrointestinal acquisition of Mucorales is well documented and greenhouse workers handle contaminated material constantly, though it may equally have been an incidental finding that contributed to the dangerous delay.

On admission, the man was alert, oriented, and afebrile, with intact vision and no cranial nerve deficits, findings that could easily have reassured clinicians. But computed tomography and magnetic resonance imaging of his sinuses and orbits told a more alarming story: right-sided proptosis, meaning the eye was being pushed forward, together with significant edema and infiltration of both the intraconal and extraconal fat spaces inside the orbit. T2-weighted MRI sequences showed the bright signal characteristic of acute inflammatory change, though without definite evidence of intracranial extension or cavernous sinus thrombosis. Such imaging findings are non-specific and can appear in severe bacterial cellulitis, but the combination of rapid deterioration, extensive orbital involvement, and the patient’s occupational history in a high-risk environment raised immediate suspicion of invasive fungal disease and guided the urgent biopsy that followed.

The laboratory work-up was equally revealing for what it did not find. The patient’s white blood cell count was mildly elevated at 12.6 × 10³ per microliter with 95 percent neutrophils, C-reactive protein stood at 37 mg/L, and his erythrocyte sedimentation rate was 21 mm/h, all consistent with a robust systemic inflammatory response. Yet targeted immunological testing, including HbA1c of 5.3 percent, negative HIV serology, and normal immunoglobulin G, A, and M levels, confirmed that he was genuinely immunocompetent. His fasting glucose of 110 mg/dL represented only an impaired fasting glucose, a subtle metabolic derangement. The authors note that even mild hyperglycemia can upregulate endothelial receptors such as GRP78, enhancing fungal adhesion and angioinvasion, and emerging evidence suggests that transient or subclinical dysglycemia can predispose otherwise healthy individuals to opportunistic mycoses.

Definitive diagnosis came from the mycology laboratory. During drainage of the eye discharge, necrotic tissue and purulent secretions were sampled and examined under potassium hydroxide preparation, hematoxylin and eosin staining, and Giemsa staining. All three revealed the pathognomonic signature of Mucorales: broad, aseptate, ribbon-like hyphae branching at wide angles. Culture on Sabouraud dextrose agar produced luxuriant, fluffy, grayish-white to brown colonies within seven days at 30 degrees Celsius, and lactophenol cotton blue microscopy of the isolate, showing sporangiophores with rhizoids at their base and a columella, identified the culprit as a Rhizopus species. Repeat sampling from the skull base again yielded positive results. Critically, treatment was initiated on the basis of microscopy alone, because fungal culture sensitivity is only 30 to 50 percent and its slow turnaround makes it useless for guiding urgent therapy.

What followed was an aggressive multimodal assault on the infection. Surgeons performed an urgent orbital exenteration, the radical removal of the entire contents of the eye socket, after intraoperative inspection revealed extensive necrotic tissue that had to be excised to prevent extension to the skull base, a complication carrying a mortality above 80 percent. Simultaneously, the patient received intravenous liposomal amphotericin B at 5.0 to 10 mg/kg per day, continued for a total of three weeks. The combined medical-surgical approach was well tolerated and produced a favorable clinical response. He was discharged in stable condition upon completing the antifungal course, and final culture results corroborated the diagnosis seven days after discharge. At follow-up three months later, he remained asymptomatic with no signs of recurrence, though he has been counseled on occupational safety measures should he return to greenhouse work.

The case fits a growing pattern in which occupational and environmental exposure, rather than host immunosuppression, precipitates invasive disease. A cohort study of cucumber greenhouse workers documented substantial exposure to airborne fungi, including Mucorales species, using next-generation sequencing alongside biomarkers of systemic inflammation, lending biological plausibility to the exposure route even though invasive disease was not observed in that cohort. Comparable risk has been described after natural disasters, including a case of rhino-orbital mucormycosis in an immunocompetent adult following prolonged mold exposure during post-hurricane cleanup, and rural living or contact with organic matter has been implicated in pediatric orbital mucormycosis without underlying immunodeficiency. The authors argue that a sufficiently high inoculum of spores can simply overwhelm innate defenses, particularly phagocytosis by neutrophils and macrophages, which are typically effective against Mucorales.

A literature search across PubMed, Scopus, and Web of Science covering January 2000 to October 2025, summarized by the authors, shows how consistently diagnostic delay haunts immunocompetent patients. A 67-year-old woman who developed headache, diplopia, and vision loss after post-hurricane mold cleanup recovered fully after multiple debridements and amphotericin B. A 12-year-old girl with a nasal foreign body and Rhizopus oryzae infection survived after surgery and antifungal therapy, as did a 22-year-old man with a minor skin lesion who required exenteration. But a 59-year-old woman with no identified risk factors died of multiple organ failure, diagnosed only at post-mortem, and a 32-year-old man died after treatment non-compliance, a reminder that even favorable biology depends on adherence to therapy. Across these reports, the absence of classic risk factors and the non-specific nature of early symptoms repeatedly misled clinicians.

For physicians on the front lines, the message is stark: progressive orbital infections deserve consideration of mucormycosis even in patients with no diabetes, no malignancy, and no immunosuppressive drugs, particularly when their work or environment involves soil, decaying vegetation, or mold-laden air. Interestingly, angioinvasion in immunocompetent hosts may follow a somewhat less fulminant course than in diabetic patients, offering a window for recovery if clinicians act quickly. High clinical suspicion, prompt histopathological diagnosis using KOH preparations and tissue staining, and aggressive combined surgical and antifungal treatment remain the pillars of survival, with combined approaches yielding roughly 60 percent survival in rhino-orbital-cerebral disease compared with more than 90 percent mortality in disseminated infection. As greenhouse agriculture expands worldwide, this single case suggests that the boundary between harmless environmental mold and life-threatening invasion may be thinner than the immune status of the host alone would suggest.

Subject of Research: Rhino-orbital mucormycosis in an immunocompetent adult linked to occupational greenhouse mold exposure

Article Title: Rhino‐Orbital Mucormycosis in an Immunocompetent Adult: A Case Report Emphasizing Diagnostic and Therapeutic Challenges

Article References: Mousavi, S. M., Mousavi, S. A. A., Faryabi, O., Sharifi, I., Kamyab, H., & Shirazi, Z. (2026). Rhino‐Orbital Mucormycosis in an Immunocompetent Adult: A Case Report Emphasizing Diagnostic and Therapeutic Challenges. Clinical Case Reports, 14(10), Article e73683. https://doi.org/10.1002/ccr3.73683

Image Credits: AI Generated

DOI: 10.1002/ccr3.73683

Keywords: mucormycosis, Rhizopus, orbital exenteration, immunocompetent patient, greenhouse workers, occupational exposure, liposomal amphotericin B, fungal infection, angioinvasion, diagnostic delay, Mucorales, Iran

The chemistry of methylene chloride explains both its industrial appeal and its hazard. The molecule, CH2Cl2, is a tetrahedral organochlorine compound with a molecular weight of 84.93 grams per mole, a boiling point of just 39.75 degrees Celsius and a vapour pressure of roughly 350 torr at 25 degrees Celsius. That volatility means it evaporates rapidly at room temperature, producing dense fumes that accumulate in poorly ventilated spaces. It is colourless, miscible with many other solvents, and carries a sweet, chloroform-like odour that can cause olfactory fatigue, meaning workers may stop noticing it precisely when concentrations become dangerous. Because the compound is denser than air, it can pool in low-lying or enclosed areas, creating suffocation hazards. Anhydrous methylene chloride is non-corrosive to most common metals, but hydrolysis produces hydrochloric acid, which attacks iron and aluminium, so commercial formulations include stabilizers such as propylene oxide, hydroquinone or cyclohexane to limit decomposition.

Industrially, the compound is manufactured by chlorinating methane or methyl chloride at temperatures around 400 to 500 degrees Celsius, a radical reaction that yields a mixture of chloromethanes separated by distillation. Its applications are remarkably broad: paint and varnish stripping, metal degreasing, polyurethane foam blowing, pharmaceutical processing, polycarbonate plastics production, electronics manufacturing, and even decaffeination of coffee, where the US Food and Drug Administration permits residual levels of about 10 parts per million. The Asia-Pacific region, driven by China, India, Japan and South Korea, now constitutes the largest market, fueled by demand for paints, coatings and generic medicines. India alone, which supplies roughly 20 percent of the world’s generic drugs, hosts approximately 3,000 pharmaceutical companies operating more than 10,500 manufacturing facilities, many of which rely on methylene chloride as a process solvent.

Environmental monitoring reveals just how pervasive the chemical has become. About 80 percent of all methylene chloride produced is ultimately released into the atmosphere, where surveys have detected ambient concentrations ranging from zero to 570 micrograms per cubic metre in the United States and up to 9.9 micrograms per cubic metre in Canada. Indoor air can be far worse: in poorly ventilated rooms, concentrations between 460 and 2,980 micrograms per cubic metre have been recorded, and household products such as paint removers and adhesives can generate exposure levels of 15 to 1,770 milligrams per cubic metre during use. The compound also appears in municipal drinking water at 1.1 to 2.0 micrograms per litre, forms as a byproduct of water chlorination, and has been measured in the River Rhine. Food products including spice oleoresins, fumigated grains, seafood, butter and cheese carry trace amounts. Soil and sediment samples from hundreds of hazardous waste sites contain detectable levels, with a geometric mean concentration of about 104 parts per billion.

Once inhaled or ingested, methylene chloride is absorbed rapidly through the lungs and gastrointestinal tract and distributed throughout the body, crossing the blood-brain barrier and the placenta and accumulating preferentially in adipose tissue. Human volunteer studies show that roughly 70 to 75 percent of inhaled vapour is absorbed, with uptake increasing during exercise and in individuals with higher body fat. The compound’s toxicology hinges on two competing metabolic pathways in the liver. The dominant route involves oxidation by the microsomal cytochrome P-450 enzyme CYP2E1, which converts methylene chloride into unstable dichloromethanol, then formyl chloride, and ultimately carbon monoxide. This carbon monoxide binds haemoglobin with an affinity 210 to 270 times greater than oxygen, forming carboxyhaemoglobin, a biomarker that effectively turns methylene chloride poisoning into a slow, internal carbon monoxide poisoning. The oxidative pathway saturates at inhalation concentrations of about 500 parts per million.

The second, minor pathway involves conjugation with glutathione, catalysed by the enzyme GSTT1. Although quantitatively smaller, this route may be the more sinister one for cancer risk: it produces formaldehyde, formic acid and S-chloromethyl glutathione, an electrophile that binds nucleophilic sites on DNA. Studies indicate that the GST pathway is more active in mice and rats than in humans and hamsters, which complicates extrapolation from rodent tumour data, yet the pathway shows no saturation even at inhalation concentrations of 10,000 parts per million. Chronic inhalation studies in mice have produced malignant lung and liver tumours, and rats developed benign and malignant tumours of the lung, liver and mammary gland. Human epidemiological evidence, particularly an increased incidence of biliary tract tumours among workers exposed to methylene chloride alongside 1,2-dichloropropane, drove the IARC’s revision of its carcinogenic classification, and the compound has been linked to cholangiocarcinoma in humans.

Acute exposures tell a grim clinical story. Case reports document a 16-year-old who developed Goodpasture’s syndrome after inhaling solvent vapours at work, a 19-year-old suffering acute tubular necrosis and liver enzyme elevations, and an art student who collapsed within an hour of exposure with a carboxyhaemoglobin level of 50 percent. Perhaps most chilling is the case of a painter who used a methylene chloride-based paint remover in a poorly ventilated room containing a kerosene stove; the combination released lethal phosgene gas, and the painter died within 12 hours. Dermal contact is equally hazardous, producing painful chemical burns that destroy epidermal and dermal lipids, with documented cases of workers left unconscious while partially immersed in the liquid. Because carbon monoxide generated by metabolism continues to form after exposure ends, carboxyhaemoglobin levels can keep rising for one to two hours, and the half-life of carboxyhaemoglobin after methylene chloride exposure extends to about 13 hours, far longer than the 5.3 hours typical after direct carbon monoxide poisoning.

Treatment mirrors carbon monoxide management: immediate removal from exposure, high-flow oxygen therapy and, in severe cases, hyperbaric oxygen, which can shorten the carboxyhaemoglobin half-life to 15 to 20 minutes under 2.5 atmospheres of pressure. Prevention, however, remains the better strategy, and regulators have responded incrementally over decades. NIOSH set an initial exposure limit of 75 parts per million in 1976, later urging minimal exposure after recognizing tumorigenic potential. OSHA tightened its standard from 500 to 25 parts per million over an eight-hour shift, with a short-term limit of 125 parts per million for 15 minutes. The FDA banned methylene chloride in cosmetics and hairsprays in 1989, and in 2019 the EPA issued a final rule banning the manufacture and distribution of methylene chloride paint strippers for retail sale after a series of occupational fatalities. Recommended workplace controls include dedicated ventilated chambers, supplied-air respirators, fume hoods, corrosion-resistant storage containers, personal protective equipment and strict segregation of food and drink from solvent areas.

Encouragingly, viable alternatives are now entering the market. AcraStrip, a semi-aqueous, non-flammable and biodegradable paint-stripping solvent, offers recyclability and zero harmful vapours. Infrared light-wave strippers can loosen multiple layers of paint in 60 seconds without chemicals, while laser cleaning uses nanosecond pulses to vaporize lead and chrome-based coatings with minimal secondary waste. Chemical substitutes include dimethyl carbonate, N-methyl-2-pyrrolidone, propylene carbonate, citrus-based cleaners and bio-derived solvents, alongside purely mechanical methods such as abrasive blasting and scraping. Waste treatment technologies, including UV, UV-titanium dioxide and biotrickling reactors, can convert methylene chloride in waste gas streams into water-soluble byproducts, and the compound is readily biodegraded by Pseudomonas species under both aerobic and anaerobic conditions. The review’s authors argue that green chemistry principles could eliminate methylene chloride from pharmaceutical synthesis entirely, but they caution that more research is needed into its toxicity mechanisms, its human carcinogenic potential and improved disposal techniques. Until then, the one-million-ton-per-year question remains: how long can industry afford a solvent that poisons its workers, its consumers and its atmosphere?

Subject of Research: Toxicology and carcinogenicity of the industrial solvent methylene chloride (dichloromethane), covering its sources, exposure routes, metabolism, ecological effects, regulation and alternatives

Article Title: Sources, exposure, metabolism, transportation, ecological effects, preventive measures and alternatives of carcinogenic methylene chloride: a review

Article References: Kumari, D., Janmeda, P., & Singh, D. (2024). Sources, exposure, metabolism, transportation, ecological effects, preventive measures and alternatives of carcinogenic methylene chloride: a review. Discover Toxicology, 1(1), Article 15. https://doi.org/10.1007/s44339-024-00012-8

Image Credits: AI Generated

DOI: 10.1007/s44339-024-00012-8

Keywords: methylene chloride, dichloromethane, carcinogen, volatile organic compound, carbon monoxide, cytochrome P-450, glutathione S-transferase, occupational exposure, paint strippers, environmental pollution, green chemistry, solvent alternatives