Metabolic syndrome has been associated in many studies with working in shifts. Even if the mechanistic details are not fully understood, forced sleep deprivation and exposure to light, as happens during night shifts, or irregular schedules with late or very early onset of the working program, lead to a sleep–wake rhythm misalignment, metabolic dysregulation and oxidative stress. The cyclic melatonin secretion is regulated by the hypothalamic suprachiasmatic nuclei and light exposure. At a central level, melatonin promotes sleep and inhibits wake-signals. Beside this role, melatonin acts as an antioxidant and influences the functionality of the cardiovascular system and of different metabolic processes. This review presents data about the influence of night shifts on melatonin secretion and oxidative stress. Assembling data from epidemiological, experimental and clinical studies contributes to a better understanding of the pathological links between chronodisruption and the metabolic syndrome related to working in shifts.

Background: Occupational exposure accounts for the second preventable risk factor for bladder cancer (BC), after smoking.Objective: This study aimed to extract evidence-based data from the systematic reviews that included studies primarily from the past 30 years, based on a clearly defined method of exposure assessment.Methods: A literature search in PubMed, Web of Science, ScienceDirect, and Embase was conducted using variations of the keywords “BC,” “occupational exposure,” and/or “occupation.” The inclusion criteria for the umbrella review were the following: systematic reviews and meta-analyses focused on occupational exposure, with a clear definition of the exposure assessment, a risk estimate for BC, and a majority of data from 1993 to 2023. We did not include other forms of reviews or systematic reviews focused on the general population and environmental exposure. Data were synthesized based either on occupations or on occupational hazards. After the overlap checking, the remaining reviews were assessed for quality using AMSTAR 2 criteria and afterwards classified for high, moderate, or low evidence using the GRADE scale.Results: We found relevant associations with a high level of evidence for firefighters, hairdressers, painters, workers in the petroleum industry, and dry cleaners exposed to tetrachloroethylene. Concerning hazards, exposure to ortho-toluidine was also confirmed to be a risk by recent studies. Welders, veterans, and those exposed to hexavalent chromium at higher risk need more well-designed studies to be confirmed.Conclusion: Despite longstanding recognition of certain risks, occupational exposure remains insufficiently investigated. Recent data support the inclusion of occupations and hazards in the individual risk assessment for BC.

Background/Objectives: Long COVID, characterized by persistent symptoms following SARS-CoV-2 infection, poses a significant occupational health concern among healthcare workers (HCWs). This study aimed to evaluate the prevalence of long COVID, symptom patterns, work-related impact, and vaccination status among healthcare personnel in a Romanian pediatric hospital. Methods: A cross-sectional study was conducted in 2024 among 903 hospital employees during routine occupational health assessments. Data were collected using structured questionnaires and medical records, focusing on previous SARS-CoV-2 infection, vaccination status, persistent symptoms, and functional impact. Results: Long COVID was identified in 28.6% of participants, with excessive fatigue (53.5%), musculoskeletal pain, respiratory difficulties, and cognitive complaints being the most common symptoms. Staff with chronic comorbidities or increased exposure risk had significantly higher rates of functional impairment. Fewer reinfections were reported among vaccinated individuals; however, vaccination was not significantly associated with the presence of long COVID symptoms. Older age and comorbidities were correlated with higher risk. Conclusions: The findings underline the need for long-term occupational health strategies and individualized support programs for HCWs affected by long COVID, particularly in high-risk groups.

Introduction Occupational cancer is a major public health issue and continuous efforts are developed all around the world to find better solutions to decrease this prevalence. This is important in particular for the persons diagnosed earlier, as they might have different prognosis and health-related quality of life. Objectives The main objective of the study is to present the prevalence of the early diagnosed lung cancer in different activity domains and possible factors associated to a younger age recognition. Methods This is a secondary analysis of data collected during the ROMCAN project (reference/acknowledgements). From the whole data-base we have received only anonymized data concerning lung cancer. Age, gender, level of education, occupational domain, smoking, personal medical history, family history of cancer was included in the analysis. Based on the distribution of age in the whole sample, we considered the early diagnosis any diagnosis before 56 years of old; the others were considered the control group. Among the demographic factors only education seems to be of influence (χ ² =31.24, p< 0.001). Family history was more prevalent in the earlier diagnosed group (OR=1.4, p=0.009). In terms of occupational domains, the highest prevalence at younger age was in the leather industry (57.14%), trade services (42.22%), extractive industry (34.62%) wood and furniture (34.48%) domains. Conclusions Occupational exposure to carcinogens contributes to the early development of lung cancer but other elements (smoking, socio-economic level, comorbidities), have also a significant role. Based on these results, awareness related to lung cancer in extractive, leather, wood manufactures and trade should be re-in forced.

Introduction: For lung cancer, the total interval time to diagnosis (TITD) is very important. If not detected by the screening program, the actual guidelines emphasize the need for a short delay to assure the initiation of treatment before 2 months from the initial symptoms. In order to shorten TITD, the individual risk has to be properly assessed by the primary physician. Objective: The assessment of the influence of the occupational exposure on the diagnostic delay—from the onset of symptoms to confirmed diagnosis—in a population of patients with lung cancer. Material and methods: A total of 110 cases were recruited and were divided into two groups based on the individual assessment by an occupational physician. Results: There were 38 cases (34.55%) at high risk according to their occupational exposure and 72 controls. On average, the TITD was 3.41 +/−5.12 months. The TITD was significantly longer in the high-risk group (p = 0.03). A larger proportion cases had longer TITD: 55.17% of cases vs. 44.83% of controls (p = 0.006). In a multivariate analysis including covariates’ age, sex, level of education, health literacy, number of packs-years, family history of cancer, and previous lung diseases associated with a high risk of lung cancer, the highest risk derived from the previous occupational exposure was the only variable statistically associated with TITD (OR = 10.57, 2.06–54.34, p = 0.01). Discussion: Awareness about the occupational risk in workers who are or have been exposed and in health providers could reduce the total interval time to diagnosis.

Background: Targeted therapies directed against oncogenic drivers have substantially improved outcomes for patients with epidermal growth factor receptor (EGFR)-mutant and anaplastic lymphoma kinase (ALK)-rearranged non-small cell lung cancer (NSCLC). Despite high initial response rates, most patients ultimately develop acquired resistance to tyrosine kinase inhibitors (TKIs), reflecting complex biological adaptations under therapeutic pressure. Methods: This narrative review synthesizes experimental, translational, and clinical studies examining how environmental and occupational respiratory exposures may influence resistance mechanisms in EGFR- and ALK-driven NSCLC. The review emphasizes exposure-associated signaling plasticity, inflammatory microenvironmental modulation, metabolic reprogramming, and pharmacokinetic alterations. Results: Recent evidence suggests that respiratory exposures, including cigarette smoke, air pollution, diesel exhaust, and occupational inhalational toxicants, can modulate oncogenic signaling networks relevant to resistance to targeted therapies. These mechanisms include aberrant EGFR activation, bypass signaling through the mesenchymal–epithelial transition receptor (MET) and SRC pathways, epithelial–mesenchymal transition (EMT), adaptive kinome remodeling, and exposure-associated inflammatory signaling, all of which may influence tumor evolution and therapeutic response. Conclusions: This review introduces a novel exposome-driven conceptual framework integrating environmental exposures with signaling plasticity and resistance evolution in oncogene-driven NSCLC. These findings support the concept that the respiratory exposome may represent an underrecognized modifier of targeted therapy response. Incorporating structured exposure assessment into precision oncology approaches may refine risk stratification and inform exposure-aware therapeutic strategies.