Radon exposure and potential health effects other than lung cancer: a systematic review and meta-analysis.

Context and objective: To date, lung cancer is the only well-established health effect associated with radon exposure in humans. To summarize available evidence on other potential health effects of radon exposure, we performed a comprehensive qualitative and quantitative synthesis of the available literature on radon exposure and health effects other than lung cancer, in both occupational and general populations. Method: Eligible studies published from January 1990 to March 2023, in English and French languages, were identified in PubMed, ScienceDirect, Scopus, ScieLo and HAL. In the meta-analysis, we estimated average weighted standardized incidence ratios (metaSIR), standardized mortality ratios (metaSMR), and risk ratio (metaRR) per 100 unit (Bq/m3 or Working level Month) increase in radon exposure concentration by combining estimates from the eligible studies using the random-effect inverse variance method. DerSimonian & Laird estimator was used to estimate the between-study variance. For each health outcome, analyses were performed separately for mine workers, children, and adults in the general population. Results: A total of 129 studies were included in the systematic review and 40 distinct studies in the meta-analysis. For most of these health outcomes, the results of the meta-analyses showed no statistically significant association, and heterogeneity was only present among occupational studies, especially between those included in the metaSIR or metaSMR analyses. However, the estimated exposure-risk associations were positive and close to the statistical significance threshold for: lymphohematological cancer incidence in children (metaRR = 1.01; 95%CI: 1.00-1.03; p = 0.08); malignant melanoma mortality among adults in the general population (metaRR = 1.10; 95%CI: 0.99-1.21; p = 0.07); liver cancer mortality among mine workers (metaRR = 1.04; 95%CI: 1.00-1.10; p = 0.06); intestine and rectal cancer mortality combined among mine workers (metaRR = 1.02; 95%CI: 1.00-1.04; p = 0.06). Conclusion: Although none of the exposure-risk associations estimated in the meta-analyses reached statistical significance, the hypothesis that radon may have other health effects apart from lung cancer could not be ruled-out and call for additional research. Larger and well-designed studies are needed to further investigate this question. Systematic review registration: https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42023474542, ID: CRD42023474542.

Partial role of volatile organic compounds in behavioural responses of mice to bedding from cancer-affected congeners.

Tumours induce changes in body odours. We compared volatile organic compounds (VOCs) in soiled bedding of a lung adenocarcinoma male mouse model in which cancer had (CC) versus had not (NC) been induced by doxycycline at three conditions: before (T0), after 2 weeks (T2; early tumour development), after 12 weeks (T12; late tumour development) of the induction. In an earlier study, wild-derived mice behaviourally discriminated between CC and NC soiled bedding at T2 and T12. Here, we sought to identify VOCs present in the same soiled bedding that could have triggered the behavioural discrimination. Solid phase micro-extraction was performed to extract VOCs from 3 g-sample stimuli. While wild-derived mice could discriminate the odour of cancerous mice at a very early stage of tumour development (T2), the present study did not identify VOCs that could explain this behaviour. However, consistent with the earlier behavioural study, four VOCs, including two well-known male mouse sex pheromones, were found to be present in significantly different proportions in soiled bedding of CC as compared to NC at T12. We discuss the potential involvement of non-volatile molecules such as proteins and peptides in behavioural discrimination of early tumour development (T2), and point-out VOCs that could help diagnose cancer.

Unrealistic risk perceptions of Iranian current cigarette smokers on developing lung cancer and chronic obstructive pulmonary disease (COPD): a cross-sectional study.

Cigarette smoking causes serious complications and diseases in a person's life, such as Chronic Obstructive Pulmonary Disease (COPD) and some cancers, including lung cancer. On the other hand, studies have shown that smokers do not have a real understanding of the health hazards of smoking. This study was conducted to determine the perceived risk of lung cancer and COPD in current smokers. This cross-sectional study which was conducted between January-May 2023, recruited 380 current smokers by convenience sampling in community setting. The data were collected face to face using three questionnaires (1) the risk perception for lung cancer and COPD questionnaire, (2) the smoking stage of change questionnaire, and (3) the Fagerström test for nicotine dependence. We examined the relationship between the included variables and the smokers' perceived risk of lung cancer and COPD by using multiple linear regression. We found that lower education (coefficient = 3.60, 95%CI [1.00, 6.19], P < 0.0001) for elementary level and (coefficient = 2.81, 95% CI [0.36, 5.26], P < 0.05) for secondary level had greater lung cancer perceived risk. Besides, smoking age onset for 20 + years (coefficient=-1.36, 95%CI [-2.42, -3.17], P < 0.0001) lower than those who started before the age of 20 were associated with lower perceived risk for lung cancer. Regarding COPD, results indicated that lower education (coefficient = 4.54, 95% CI [1.87, 7.21], p < 0001) for elementary level (coefficient = 3.35, 95% CI [0.83, 5.87], p < 0.001) for secondary level and (coefficient = 3.03, 95% CI[-0.67, 4.25], P < 0.05) for high school dropout, and employment status (coefficient = 3.62, 95% CI[0.66, 6.59], p < 0.05) of employer and (coefficient = 3.23, 95% CI [0.14, 6.33], p < 0.05) for homemaker reported greater perceived risk. This study's results showed that participants' perceived risk was relatively low. It seems necessary to carry out interventions to inform about the harms of smoking and to enhance public awareness about the heightened risks of diseases such as lung cancer and COPD among cigarette smokers.

Radon Risk Communication through News Stories: A Multi-Perspective Approach.

Radon is, after tobacco, the most frequent cause of lung cancer. Communicating about its risks with a didactic perspective so that citizens become aware and take action to avoid radon remains a challenge. This research is framed in Spain, where 17% of the territory exceeds the maximum radon limits allowed by the WHO, and aims to study the role and impact of the media in radon risk communication. A mixed methodological design is applied, combining content analysis of news published in the last two decades by local media in the most affected areas with interviews with journalists and a survey of citizens to provide a multi-perspective approach. The results show that, although news coverage of radon is becoming more frequent, it is a topic that fails to position itself on the agenda for effective communication. The media are the most frequent source of information on radon, although they are not considered by the public the most trustworthy one. News stories about radon focus mainly on health and research to inform about the radon levels to which citizens are exposed and the risks associated with cancer. Collaborative strategies between the media, organizations, and public administration seem key to advancing the fight against radon.

Air pollution, dysbiosis and diseases: pneumonia, asthma, COPD, lung cancer and irritable bowel syndrome.

With substantial effects on human health, air pollution has become a major global concern. Air pollution has been linked to numerous gastrointestinal and respiratory diseases with increasing mortalities. The gut and respiratory dysbiosis brought about by air pollution has recently received much attention. This review attempts to provide an overview of the types of air pollutants, their sources, their impact on the respiratory and gut dysbiotic patterns and their correlation with five major diseases including pneumonia, asthma, COPD, lung cancer and irritable bowel syndrome. Deeper insights into the links between pollutants, dysbiosis and disease may pave the way for novel diagnostic biomarkers for prognosis and early detection of these diseases, as well as ways to ease the disease burden.

Air pollution has become a major environmental concern because it can harm human health. Generally, air pollution is either classified as indoor or outdoor. Air pollutants are released from factories, automobiles, preparation of construction materials, agricultural practices, poultry and animal farming and even domestic tasks such as cooking. Air pollution can cause various illnesses of the gastrointestinal tract and lungs. These include cystic fibrosis, pneumonia, asthma, lung cancer, COPD and irritable bowel syndrome. These diseases are linked to disruptions of the community of bacteria in the lungs and gastrointestinal tract. This review looks at the impact of air pollution on microbial communities and associated diseases.

Applying a 'presumably plausible' principle in a new one-time financial compensation system for occupational diseases in the Netherlands.

OBJECTIVES: In the Netherlands, a new regulation has been adopted for recognition and compensation of serious substance-related occupational diseases. A national advisory committee has a key task of providing advice on the protocols for operationalisation of individual causality assessment in this new context. METHODS: Protocol development involves gathering the best available population-level evidence on causality and using this evidence to determine individual causality. Here, the presumably plausible principle was adopted, which stipulates that uncertainties in individual causality should be weighed in favour of a fast and transparent one-time compensation for (ex-)workers. RESULTS: In monocausal diseases, a limited workplace exposure assessment is considered sufficient to determine whether individual causality is presumably plausible in the Dutch context. For multicausal occupational diseases, individual causality assessment is more complicated. Modelling of existing data on the exposure-response relation helps establish the probability of causation, that is, the risk of the disease attributable to a work-related exposure. This operationalisation, applied in some protocols, makes use of the probability of causation, while being prudent in establishing exposure limits. An example from asbestos and lung cancer is provided in this short report. CONCLUSIONS: We propose a pragmatic approach to individual causality assessment of substance-related occupational diseases, considering statistical and diagnostic uncertainties. This approach substantiates protocols towards a one-time financial compensation without long-winding recognition procedures.

Dietary total antioxidant capacity and odds of lung cancer: a large case-control study.

BACKGROUND& AIMS: We aimed to study the association between dietary total antioxidant capacity (dTAC) and lung cancer (LC) odds in an Iranian population. METHODS: We recruited histopathologically diagnosed LC patients and healthy subjects from 10 provinces of Iran. Trained interviewers conducted face-to-face interviews using a structured questionnaire to collect demographic and other non-dietary information. Dietary habits in the previous year were evaluated using a validated food frequency questionnaire (FFQ). We calculated daily energy and nutrient intakes using the USDA Food Composition Table. DTAC was assessed as ferric reducing antioxidant power (FRAP) and total radical-trapping antioxidant parameters (TRAP) whose scores were calculated using published databases. The odd ratios (OR) of LC and 95% confidence intervals (CI) were estimated using unconditional logistic regression after adjusting for potential confounders. Moreover, we assessed the associations in stratified groups of age, gender, tobacco including waterpipe smoking, and opium use. RESULTS: Six hundered and sixty patients and 3,412 healthy controls were included in our study. Higher FRAP and TRAP scores were associated with a lower odd of LC (FRAP, upper tertile (T3) vs. lower tertile (T1): OR = 0.53, 95% CI: 0.40-0.68; TRAP, T3 vs. T1: OR = 0.44, 95% CI: 0.33-0.57) with a significant dose-response trend for both scores (p < 0.01). The inverse association was seen for both indicators in all histologic types of LC and in all stratified analyses including male/female, tobacco smokers/nonsmokers, opium users/nonusers, water pipe users/nonusers, and subjects under/over 50 years of age. However, Interaction between none of these variables with dTAC scores was significant. CONCLUSION: Higher dTAC is associated with a lower odd of LC. The strong association in all subgroups highlights the importance of an antioxidant-rich diet intake in all subjects, even in the low-risk group.

A Multi-Omics Study of Epigenetic Changes in Type II Alveolar Cells of A/J Mice Exposed to Environmental Tobacco Smoke.

Lung cancer remains a major contributor to cancer fatalities, with cigarette smoking known to be responsible for up to 80% of cases. Based on the ability of cigarette smoke to induce inflammation in the lungs and increased lung cancer incidence in smokers with inflammatory conditions such as COPD, we hypothesized that inflammation plays an important role in the carcinogenicity of cigarette smoke. To test this hypothesis, we performed multi-omic analyses of Type II pneumocytes of A/J mice exposed to cigarette smoke for various time periods. We found that cigarette smoke exposure resulted in significant changes in DNA methylation and hydroxymethylation, gene expression patterns, and protein abundance that were partially reversible and contributed to an inflammatory and potentially oncogenic phenotype.

The effect of air pollution quality on lung cancer rates in middle-income and high-income countries: a panel data analysis approach.

Background: Air pollution is one of the biggest problems in societies today. The intensity of indoor and outdoor air pollutants and the urbanization rate can cause or trigger many different diseases, especially lung cancer. In this context, this study's aim is to reveal the effects of the indoor and outdoor air pollutants, and urbanization rate on the lung cancer cases. Methods: Panel data analysis method is applied in this study. The research includes the period between 1990 and 2019 as a time series and the data type of the variables is annual. The dependent variable in the research model is lung cancer cases per 100,000 people. The independent variables are the level of outdoor air pollution, air pollution level indoor environment and urbanization rate of countries. Results: In the modeling developed for the developed country group, it is seen that the variable with the highest level of effect on lung cancer is the outdoor air pollution level. Conclusions: In parallel with the development of countries, it has been determined that the increase in industrial production wastes, in other words, worsening the air quality, may potentially cause an increase in lung cancer cases. Indoor air quality is also essential for human health; negative changes in this variable may negatively impact individuals' health, especially lung cancer.

Global burden of lung cancer in women of childbearing age attributable to ambient particulate matter pollution: 1990-2021.

BACKGROUND: This study aimed to evaluate the global burden of lung cancer due to ambient particulate matter (PM) pollution in women of childbearing age from 1990 to 2021. METHODS: This was a secondary analysis utilizing data from the Global Burden of Disease (GBD) 2021, with a focus on the temporal trends of the lung cancer burden attributable to ambient PM2.5 among women of childbearing age. RESULTS: In 2021, the global mortality and disability-adjusted life years (DALYs) number of lung cancer burden attributable to ambient PM2.5 among women of childbearing age were approximately 5205 and 247,211, respectively. The rate of lung cancer attributable to ambient PM2.5 among women of childbearing age increased between 1990 and 2021, with the age-standardized mortality rate (ASMR) increasing from 0.22 (95% uncertainty interval [UI]; 0.13 to 0.33) to 0.25 (95% UI; 0.14 to 0.37; average annual percent change [AAPC] = 0.40) and the age-standardized DALYs rate (ASDR) increasing from 10.39 (95% UI; 5.96 to 15.72) to 12.06 (95% UI; 6.83 to 17.51; AAPC = 0.41). The middle sociodemographic index (SDI) region, East Asia, and China had the heaviest burden, while the high SDI region showed the highest decrease. ASMR and ASDR exhibited an inverted U-shaped relationship with the SDI. CONCLUSIONS: From 1990 to 2021, the lung cancer burden attributable to ambient PM2.5 among women of childbearing age exhibited an increasing trend. Furthermore, increasing attention should be paid to the middle SDI region, East Asia, and China, as ambient PM pollution remains a critical target for intervention.

The Association between Allergy and Cancer: A Case-Control Study.

BACKGROUND: Allergies may either have a protective or a promoting effect on cancers. This study seeks to explore the relationship between various types of allergies and three specific cancer types: lung, breast, and colorectal cancer, thereby adding fresh insights to the existing scientific. METHODS: Among the 556 patients, there were 115 cases of colorectal cancer, 305 cases of breast cancer, and 136 cases of lung cancer. The ratio of the case group to the control group was 1:1. We assessed the association between various variables, such as family history of allergy, allergies since the age of 10, pet allergies, seasonal flu, night and activity-related coughing, food allergies, itching or urticaria, childhood respiratory infections, and common colds, with the aforementioned cancers. The data were also analyzed using conditional logistic regression. RESULTS: The results showed a protective association between itching or urticaria due to environmental factors and colorectal cancer (adjusted odds ratio [AOR]: 0.4, 95% CI: 0.17-0.94), as well as lung cancer (AOR: 0.26, 95% CI: 0.09-0.75). Additionally, a borderline association was observed between itching or urticaria and breast cancer (AOR: 0.54, 95% CI: 0.28-1.03). Allergy to pets also exhibited an inverse borderline association with breast cancer (AOR: 0.44, 95% CI: 0.18-1.05) and lung cancer (AOR: 0.25, 95% CI: 0.06-1.14). Furthermore, night coughing and allergies since the age of 10 were found to increase the odds of developing breast cancer (AOR: 2.38, 95% CI: 1.44-3.92; AOR: 5.10, 95% CI: 2.56-10.56, respectively) and lung cancer (AOR: 2.40, 95% CI: 1.29-4.46; AOR: 8.71, 95% CI: 3.29-23.03, respectively). CONCLUSION: allergies and cancer have a site-specific assciation . To confirm these findings and understand the reasons behind these associations, more investigation is required.

Beyond tobacco: genomic disparities in lung cancer between smokers and never-smokers.

BACKGROUND: Tobacco use is one of the main risk factors for Lung Cancer (LC) development. However, about 10-20% of those diagnosed with the disease are never-smokers. For Non-Small Cell Lung Cancer (NSCLC) there are clear differences in both the clinical presentation and the tumor genomic profiles between smokers and never-smokers. For example, the Lung Adenocarcinoma (LUAD) histological subtype in never-smokers is predominately found in young women of European, North American, and Asian descent. While the clinical presentation and tumor genomic profiles of smokers have been widely examined, never-smokers are usually underrepresented, especially those of a Latin American (LA) background. In this work, we characterize, for the first time, the difference in the genomic profiles between smokers and never-smokers LC patients from Chile. METHODS: We conduct a comparison by smoking status in the frequencies of genomic alterations (GAs) including somatic mutations and structural variants (fusions) in a total of 10 clinically relevant genes, including the eight most common actionable genes for LC (EGFR, KRAS, ALK, MET, BRAF, RET, ERBB2, and ROS1) and two established driver genes for malignancies other than LC (PIK3CA and MAP2K1). Study participants were grouped as either smokers (current and former, n = 473) or never-smokers (n = 200) according to self-report tobacco use at enrollment. RESULTS: Our findings indicate a higher overall GA frequency for never-smokers compared to smokers (58 vs. 45.7, p-value < 0.01) with the genes EGFR, KRAS, and PIK3CA displaying the highest prevalence while ERBB2, RET, and ROS1 the lowest. Never-smokers present higher frequencies in seven out of the 10 genes; however, smokers harbor a more complex genomic profile. The clearest differences between groups are seen for EGFR (15.6 vs. 21.5, p-value: < 0.01), PIK3CA (6.8 vs 9.5) and ALK (3.2 vs 7.5) in favor of never-smokers, and KRAS (16.3 vs. 11.5) and MAP2K1 (6.6 vs. 3.5) in favor of smokers. Alterations in these genes are comprised almost exclusively by somatic mutations in EGFR and mainly by fusions in ALK, and only by mutations in PIK3CA, KRAS and MAP2K1. CONCLUSIONS: We found clear differences in the genomic landscape by smoking status in LUAD patients from Chile, with potential implications for clinical management in these limited-resource settings.

On the informative value of community-based indoor radon values in relation to lung cancer.

BACKGROUND: Radon is a radioactive gas and a major risk factor for lung cancer (LC). METHODS: We investigated the dose-response relationship between radon and LC risk in the International Lung Cancer Consortium with 8927 cases and 5562 controls from Europe, North America, and Israel, conducted between 1992 and 2016. Spatial indoor radon exposure in the residential area (sIR) obtained from national surveys was linked to the participants' residential geolocation. Parametric linear and spline functions were fitted within a logistic regression framework. RESULTS: We observed a non-linear spatial-dose response relationship for sIR < 200 Bq/m3. The lowest risk was observed for areas of mean exposure of 58 Bq/m3 (95% CI: 56.1-59.2 Bq/m3). The relative risk of lung cancer increased to the same degree in areas averaging 25 Bq/m3 (OR = 1.31, 95% CI: 1.01-1.59) as in areas with a mean of 100 Bq/m3 (OR = 1.34, 95% CI: 1.20-1.45). The strongest association was observed for small cell lung cancer and the weakest for squamous cell carcinoma. A stronger association was also observed in men, but only at higher exposure levels. The non-linear association is primarily observed among the younger population (age < 69 years), but not in the older population, which can potentially represent different biological radiation responses. CONCLUSIONS: The sIR is useful as proxy of individual radon exposure in epidemiological studies on lung cancer. The usual assumption of a linear, no-threshold dose-response relationship, as can be made for individual radon exposures, may not be optimal for sIR values of less than 200 Bq/m3.

Lung cancer caused by asbestos: What a reporting pathologist needs to know.

Asbestos is a carcinogen that can cause lung cancer. The suspicion that a lung cancer diagnosis may be associated with exposure to asbestos has no bearing on treatment. However, attributing an individual's lung cancer to asbestos exposure has important medicolegal implications and may impact public health measures and policy. Simultaneous exposure(s) to other carcinogens (such as tobacco smoke, silica and many others) adds complexity while trying to answer the causation question. The Helsinki criteria were formulated to assist attributing lung cancer to previous asbestos exposure. Surrogate markers can be used and include signs of asbestosis and pleural plaques. The most widely used criterion for the presence of asbestosis is interstitial fibrosis in conjunction with 2 or more asbestos bodies/1 cm2 tissue section by light microscopy. Identification of asbestos bodies ty light pr electron microscopy provides an important element for asbestos diagnosis. However, fibrosis may be subtle, and the distribution of asbestos bodies is not uniform throughout the lungs, some types of asbestos fibres have low biopersistence, and not all types of asbestos readily form asbestos bodies. Additional criteria require knowledge of exposure history, which is often unknown to pathologists, but reliance on morphology in isolation may lead to mis-classification of interstitial lung disease as idiopathic. While a smoking-related lung cancer signature has emerged, an asbestos-related lung cancer signature has not yet been identified. In this review we will discuss practice points for the surgical pathologist.

Asbestos Surveillance Program Aachen (ASPA): Cancer mortality among asbestos exposed power industry workers.

BACKGROUND: The time between initial asbestos exposure and asbestos-related disease can span several decades. The Asbestos Surveillance Program aims to detect early asbestos-related diseases in a cohort of 8,565 power industry workers formerly exposed to asbestos. RESEARCH QUESTION: How does asbestos exposure patterns affect cancer mortality and the duration of latency until death? METHODS: A mortality follow-up was conducted with available vital status for 8,476 participants (99 %) and available death certificates for 89.9 % of deceased participants. Standardised mortality ratios (SMR) were calculated for asbestos-related cancers. The SMR of mesothelioma and lung cancer were stratified by exposure duration, cumulative asbestos exposure and smoking. The effect of age at first exposure, cumulative asbestos exposure and smoking on the duration of latency until death was examined using multiple linear regression analysis. RESULTS: The mortality risk of mesothelioma (n = 104) increased with cumulative asbestos exposure but not with exposure duration; the highest mortality (SMR: 23.20; 95 % CI: 17.62-29.99) was observed in participants who performed activities with short extremely high exposures (steam turbine revisions). Lung cancer mortality (n = 215) was not increased (SMR: 1.03; 95 % CI: 0.89-1.17). Median latency until death was 46 (15-63) years for mesothelioma and 44 (15-70) years for lung cancer and deaths occurred between age 64 and 82 years. Latency until death was not influenced by age at first exposure, cumulative exposure, or smoking. CONCLUSION: Cumulative dose seems to be more appropriate than exposure duration for estimating the risk of mesothelioma death. Additionally, exposure with high cumulative doses in short time should be considered. Since only lung cancer mortality, not incidence, was recorded in this study, lung cancer risk associated with asbestos exposure could not be assessed and the lung cancer mortality was lower than expected probably due to screening effects and improved treatments. The critical time window of death from asbestos-related cancer is between the seventh and ninth decade of life. Future studies should further explore the concept of latency, especially since large ranges are reported throughout the literature.

Trends in Asbestos Exposure and Malignant Mesothelioma Incidence in Emilia-Romagna Italy: A Retrospective Study 1996-2023.

Malignant mesothelioma (MM) is a rare but lethal cancer strongly associated with asbestos exposure. This retrospective study examines trends in asbestos exposure in Emilia-Romagna, Northern Italy. Between 1996 and 2023, 3,513 cases of MM were recorded, predominantly in males (72%) and in older than 65 years (79%). Occupational exposure accounted for 82% of cases, with a significant increase observed over time from 71% to 88% in the most recent period. A greater definition of professional exposure indicates that certain exposure has gone from 49% in the first period to 62% and 58% in the last two periods; probable exposure showed a decrease from 21% to 16% while possible exposure decreased from 16% to 13%. Familiar exposure remained relatively constant at around 8%, environmental exposure showed a slight decrease from 4% to 2%, while non-occupational exposure remained stable at 2%. Among patients with exclusively occupational exposure (1,826 cases), 87% were male and aged between 65 and 75 years (36%) and 75+ (41%). The exposure rates for the province of residence see the province of Reggio Emilia with the highest occupational exposure rate (2.5 x 100,000 residents), followed by Ravenna (2.3 x 100,000 residents) and Parma and Piacenza which have similar exposure rates with 2.2 x 100,000 residents. Professional sectors such as construction, railway maintenance and metalworking are identified as high-risk industries. Despite efforts to mitigate exposure, non-occupational and environmental exposures persist. The study highlights the importance of continuous surveillance and exposure monitoring to guide effective interventions and legal recognition of MM.

Mortality follow-up of Fernald Feed Materials Production Center workers exposed to uranium from 1951 to 1985.

OBJECTIVE: This follow-up study of uranium processing workers at the Fernald Feed Materials Production Center examines the relationship between radiation exposure and cancer and non-cancer mortality among 6403 workers employed for at least 30 days between 1951 and 1985. METHODS: We estimated cumulative, individual, annualised doses to 15 organs/tissues from external, internal and radon exposures. Vital status and cause of death were ascertained in 2017. The analysis employed standardised mortality ratios, Cox proportional hazards and Poisson regression models. Competing risk analysis was conducted for cardiovascular disease (CVD) mortality risk given several assumptions about risk independent of competing outcomes. Emphysema was examined to assess the potential for confounding by smoking. RESULTS: Vital status was confirmed for 98.1% of workers, with 65.1% deceased. All-cause mortality was less than expected in salaried but not hourly workers when compared with the US population. A statistically significant dose response was observed between external (but not total or internal) lung dose and lung cancer mortality (HR at 100 mGy adjusted for internal dose=1.45; 95% CI=1.05 to 2.01). Significantly increased HRs at 100 mGy dose to heart were observed for CVD (1.27; 95% CI=1.07 to 1.50) and ischaemic heart disease (1.30; 95% CI=1.07 to 1.58). CVD risk remained elevated regardless of competing risk assumptions. Both external and internal radiation were associated with emphysema. CONCLUSIONS: Lung cancer was associated with external dose, though positive dose responses for emphysema imply residual confounding by smoking. Novel use of competing risk analysis for CVD demonstrates leveraging retrospective data for future risk prediction.

Clinical investigation of former workers exposed to asbestos: the health surveillance experience of an Italian University Hospital.

Background: The need for health surveillance of former workers exposed to asbestos was provided by law in Italy after the asbestos ban in 1992. Objectives: We describe the results of the health surveillance of former workers exposed to asbestos, conducted over 27 years, from 1994 to 2020, at the Operative Unit of Occupational Medicine of the University Hospital of Bari. Materials and methods: We adopted the health surveillance protocol, which was validated at the national level in 2018. Results: A total of 1,405 former workers exposed to asbestos were examined. We proceeded with diagnosing pathologies in 339 cases (24% of the cohort subjected to surveillance), with diagnoses of some cases involving multiple pathologies. Specifically, pleural plaques were diagnosed in 49.2% of the 339 cases, asbestosis in 35.9%, malignant pleural mesothelioma (MPM) in 20.3%, mesothelioma of the vaginal tunic of the testis (MTVT) in 9.1%, lung cancer in 5.8%, and laryngeal cancer in 0.8%. Conclusion: Despite the 1992 asbestos ban, asbestos-related diseases remain a serious public health issue. It is important to establish criteria that ensure the health surveillance of formerly exposed workers minimizes costs, reduces the number of invasive examinations, and optimizes achievable results.

A systematic review and dose-response meta-analysis of prospective cohort studies on coffee consumption and risk of lung cancer.

Studies on the association between coffee consumption and risk of lung cancer have been conflicting. The aim of this study was to systematically review the current evidence on the association between coffee consumption and risk of lung cancer and to quantify this association by performing a meta-analysis. A comprehensive systematic search was performed on online databases up to July 2023 investigating the association between coffee consumption and risk of lung cancer. All prospective cohort studies reporting odds ratios (ORs), rate or risk ratios (RRs), or hazard ratios (HRs) and 95% confidence intervals (CIs) in this context were included. The overall effect size was calculated using the random-effects model and statistical between-studies heterogeneity was examined using Cochrane's Q test and I2. A total of 14 prospective cohort studies were included in this systematic review and meta-analysis. We found a significant positive association between coffee consumption and risk of lung cancer (RR: 1.28; 95% CI: 1.12, 1.47). This association remained significant when we included a pooled analysis paper and excluded 5 cohort studies (RR: 1.37; 95% CI: 1.12, 1.66). We observed no proof of significant publication bias using Egger's test (P = 0.58). Moreover, dose-response analysis showed that each one cup/day increase in coffee consumption was related with a 6% higher lung cancer risk (RR: 1.06; 95% CI: 1.03, 1.09). In conclusion, we found a significant positive association between coffee consumption and risk of lung cancer.

Beyond lung cancer: air pollution and bladder, breast and prostate cancer incidence.

BACKGROUND: The carcinogenicity of air pollution and its impact on the risk of lung cancer is well known; however, there are still knowledge gaps and mixed results for other sites of cancer. METHODS: The current study aimed to evaluate the associations between ambient air pollution [fine particulate matter (PM2.5) and nitrogen oxides (NOx)] and cancer incidence. Exposure assessment was based on historical addresses of >900 000 participants. Cancer incidence included primary cancer cases diagnosed from 2007 to 2015 (n = 30 979). Cox regression was used to evaluate the associations between ambient air pollution and cancer incidence [hazard ratio (HR), 95% CI]. RESULTS: In the single-pollutant models, an increase of one interquartile range (IQR) (2.11 µg/m3) of PM2.5 was associated with an increased risk of all cancer sites (HR = 1.51, 95% CI: 1.47-1.54), lung cancer (HR = 1.73, 95% CI: 1.60-1.87), bladder cancer (HR = 1.50, 95% CI: 1.37-1.65), breast cancer (HR = 1.50, 95% CI: 1.42-1.58) and prostate cancer (HR = 1.41, 95% CI: 1.31-1.52). In the single-pollutant and the co-pollutant models, the estimates for PM2.5 were stronger compared with NOx for all the investigated cancer sites. CONCLUSIONS: Our findings confirm the carcinogenicity of ambient air pollution on lung cancer and provide additional evidence for bladder, breast and prostate cancers. Further studies are needed to confirm our observation regarding prostate cancer. However, the need for more research should not be a barrier to implementing policies to limit the population's exposure to air pollution.