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The objectives of the systematic review were to: identify the work sectors at risk for exposure to formaldehyde; investigate the procedures applied to assess occupational exposure; evaluate the reported exposure levels among the different settings. An electronic search of Pubmed, Scopus, Web of Science and ToxNet was carried out for collecting all the articles on the investigated issue published from January 1, 2004 to September 30, 2019. Forty‐three papers were included in the review, and evidenced a great number of occupational scenarios at risk for formaldehyde exposure. All the included studies collected data on formaldehyde exposure levels by a similar approach: environmental and personal sampling followed by chromatographic analyses. Results ranged from not detectable values until to some mg m−3 of airborne formaldehyde. The riskiest occupational settings for formaldehyde exposure were the gross anatomy and pathology laboratories, the hairdressing salons and some specific productive settings, such as wooden furniture factories, dairy facilities and fish hatcheries. Notice that formaldehyde, a well‐known carcinogen, was recovered in air at levels higher than outdoor in almost all the studied scenarios/activities; thus, when formaldehyde cannot be removed or substituted, targeted strategies for exposure elimination or mitigation must be adopted. [ABSTRACT FROM AUTHOR]

Background In light of recent developments in nanotechnologies, interest is growing to better comprehend the interaction of nanoparticles with body tissues, in particular within the cardiovascular system. Attention has recently focused on the link between environmental pollution and cardiovascular diseases. Nanoparticles <50 nm in size are known to pass the alveolar--pulmonary barrier, enter into bloodstream and induce inflammation, but the direct pathogenic mechanisms still need to be evaluated. We thus focused our attention on titanium dioxide (TiO2) nanoparticles, the most diffuse nanomaterial in polluted environments and one generally considered inert for the human body. Methods We conducted functional studies on isolated adult rat cardiomyocytes exposed acutely in vitro to TiO2 and on healthy rats administered a single dose of 2 mg/Kg TiO2 NPs via the trachea. Transmission electron microscopy was used to verify the actual presence of TiO2 nanoparticles within cardiac tissue, toxicological assays were used to assess lipid peroxidation and DNA tissue damage, and an in silico method was used to model the effect on action potential. Results Ventricular myocytes exposed in vitro to TiO2 had significantly reduced action potential duration, impairment of sarcomere shortening and decreased stability of resting membrane potential. In vivo, a single intra-tracheal administration of saline solution containing TiO2 nanoparticles increased cardiac conduction velocity and tissue excitability, resulting in an enhanced propensity for inducible arrhythmias. Computational modeling of ventricular action potential indicated that a membrane leakage could account for the nanoparticle-induced effects measured on real cardiomyocytes. Conclusions Acute exposure to TiO2 nanoparticles acutely alters cardiac excitability and increases the likelihood of arrhythmic events. [ABSTRACT FROM AUTHOR]

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Copyright of La Medicina del Lavoro is the property of Mattioli 1885 SpA and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Simple Summary: Formaldehyde is a chemical compound present in many working activities and indoor workplaces. Occupational exposure occurs primarily by inhaling airborne formaldehyde, but it can also be absorbed through the skin or ingested. The International Agency for Research on Cancer (IARC) classified formaldehyde as a Group 1 carcinogen for humans in 2004, based on toxicological data and epidemiological evidence obtained in workplaces, all published before that year. Over the last two decades, many new studies in this field have been published, providing updated findings. The aim of the present systematic review was to synthetize the results of epidemiological studies in occupational settings carried out in the last 20 years and to evaluate whether the IARC classification was confirmed by further studies. Our results show that the evidence of correlation between formaldehyde occupational exposure and the occurrence of cancer is limited. Background: Formaldehyde, classified as a carcinogen in 2004, as of today is widely used in many work activities. From its classification, further studies were performed to evaluate its carcinogenicity. The aim of the systematic review is to update the evidence on occupational exposure to formaldehyde and cancer onset. Methods: The review, in accordance with the PRISMA statement, includes articles in English reporting original results of studies conducted on workers exposed to formaldehyde, considering all types of cancer, published from 1 January 2000 to 30 July 2021 and selected from the Pubmed and Scopus databases. The studies' quality was assessed by the Newcastle–Ottawa Scale. Results: A total of 21 articles were included, conducted in different European, American, and Asian countries. The most investigated occupational areas are those characterized by a deliberate use of formaldehyde. Some studies evaluated all types of cancer, whereas others focused on specific sites such as thyroid and respiratory, lymphohematopoietic, or central nervous systems. The results showed weak associations with lung cancer, nasopharyngeal cancer, leukemia, and non-Hodgkin's lymphoma. Conclusions: The results demonstrate the need for further original studies carried out on representative samples of workers exposed to measured levels of FA. These studies should be designed to reduce the bias due to co-exposure to other carcinogens. [ABSTRACT FROM AUTHOR]

Abstract: Benzene is a widespread air pollutant and a well-known human carcinogen. Evidence is needed regarding benzene intake in the pediatric age group. We investigated the use of urinary (u) trans,trans-muconic acid (t,t-MA), S-phenylmercapturic acid (SPMA), and unmodified benzene (UB) for assessing exposure to low concentrations of environmental benzene and the role of living environment on benzene exposure in childhood. u-t,t-MA, u-SPMA, u-UB and u-cotinine were measured in urine samples of 243 Italian children (5–11years) recruited in a cross-sectional study. Analytical results were compared with data obtained from questionnaires about participants'' main potential exposure factors. u-UB, u-t,t-MA and u-SPMA concentrations were about 1.5-fold higher in children living in urban areas than in those in the rural group. Univariate analyses showed that u-UB was the only biomarker able to discriminate secondhand smoke (SHS) exposure in urban and rural children (medians=411.50 and 210.50ng/L, respectively); these results were confirmed by the strong correlation between u-UB and u-cotinine in the SHS-exposed group and by multivariate analyses. A regression model on u-SPMA showed that the metabolite is related to residence area (p <0.001), SHS exposure (p =0.048) and gender (p =0.027). u-UB is the best marker of benzene exposure in children in the present study, and it can be used as a good carcinogen-derived biomarker of exposure to passive smoking, especially related to benzene, when urine sample is collected at the end of the day. In addition, it is important to highlight that SHS resulted the most important contributor to benzene exposure, underlining the need for an information campaign against passive smoking exposure. [Copyright &y& Elsevier]

Abstract: A comparative evaluation of urinary biomarkers was carried out to characterize benzene exposure in a group of 100 traffic policemen of the city of Parma (Italy). All subjects were monitored once, in two consecutive days characterized by similar climatic conditions but preceded by two windy days. Benzene ambient concentration measured by municipal air monitoring stations was 1μg/m3 (Day 1) and 2μg/m3 (Day 2). Personal exposure to ambient concentrations of benzene, toluene, ethylbenzene and xylene (BTEX) was assessed by using Radiello® passive-diffusive samplers in a subgroup of 24 workers. Benzene metabolites, t,t-muconic acid (t,t-MA) and S-phenylmercapturic acid (S-PMA) were determined by isotopic dilution liquid chromatography–tandem mass spectrometry on spot urine samples collected at the end of the shift. Urinary benzene (U-B) was determined by solid-phase microextraction gas chromatography–mass spectrometry. Airborne benzene concentration expressed as median [and interquartile range] was 6.07 [0.28–9.53]μg/m3, as assessed by personal sampling. Urinary concentrations of biomarkers in the whole group were 41.8 [34.1–89.8]μg/g creatinine for t,t-MA, 0.67 [0.23–1.32]μg/g creatinine for S-PMA, and 0.16 [0.13–0.26]μg/l for U-B. Smokers eliminated significantly higher concentrations of unchanged BTEX and benzene metabolites than non-smokers (p <0.05). When traffic policemen were distinguished into indoor (n =31) and outdoor workers, no significant differences were observed for either airborne benzene or urinary biomarkers. Significantly lower concentrations of S-PMA and U-B were determined in samples collected at Day 1 as compared to Day 2 (p <0.0001 and p =0.003, respectively) suggesting that these biomarkers are enough sensitive and specific to detect changes in airborne benzene concentration even at few μg/m3. [Copyright &y& Elsevier]