Solar ultraviolet (UV) radiation follows people during their whole life. Exposure to UV radiation is vital but holds serious risks, too. The quantification of human UV exposure is a complex issue. UV exposure is directly related to incoming UV radiation as well as to a variety of factors such as the orientation of the exposed anatomical site with respect to the sun and the duration of exposure. The use of badge-sensors allows assessing the UV exposure of differently oriented body sites. Such UV devices have been available for over 40 years, and a variety of measuring campaigns have been undertaken since then. This study provides an overview of those studies which reported measurements of the personal UV exposure (PE) during outdoor activities of people not related to their occupation. This overview is given chronologically to show the progress of knowledge in this research and is given with respect to different activities. Special focus is put on the ratio of personal exposure to ambient UV radiation. This ratio, when given as a function of solar elevation, allows estimating PE at any other location or date if ambient UV radiation is known.
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http://dx.doi.org/10.1111/php.12946 | DOI Listing |
J Infect Dis
January 2025
Center for Vaccine Development and Global Health, University of Maryland School of Medicine, Baltimore, Maryland 21218, USA.
Clinical trials that employ human challenge, also known as controlled human infection models (CHIM), have rapidly advanced vaccine development for multiple pathogens, including at least 30 disease models to date. CHIM studies, championed by networks of researchers, regulators, ethicists, technical experts, and other stakeholders, limit exposure of individuals to an investigational product, de-risk product investments, identify correlates of protection, and most importantly provide a prompt readout of vaccine efficacy. While CHIM studies provide multiple advantages, important challenges exist, including strengthening the relevance and comparability of CHIM study results to efficacy trials in endemic areas, particularly in resource-limited settings.
View Article and Find Full Text PDFOccup Med (Lond)
January 2025
Maine et Loire, Univ Angers, CHU Angers, Univ Rennes, Inserm, EHESP, Irset (Institut de recherche en santé, environnement et travail) - UMR_S 1085, IRSET-ESTER, SFR ICAT, CAPTV CDC, 49000 Angers, France.
Background: Systemic sclerosis (SSc) is the connective tissue disease with the highest individual mortality. Crystalline silica is known to be an occupational risk factor for SSc. To assess past crystalline silica exposure, we aimed to study the validity of a job exposure matrix (JEM) to assess occupational exposure to crystalline silica compared to specific occupational interviews in two populations of SSc patients.
View Article and Find Full Text PDFNeurology
February 2025
Department of Neurology, University of Michigan, Ann Arbor.
Background And Objectives: An adverse social exposome negatively affects many diseases, but its association with amyotrophic lateral sclerosis (ALS) survival is unknown. This study examined the association between the social exposome measure Area Deprivation Index (ADI) and ALS survival.
Methods: This is a retrospective analysis of patients with ALS at the University of Michigan Pranger ALS Clinic diagnosed after January 1, 2012.
Am J Respir Cell Mol Biol
January 2025
The University of Texas Medical Branch at Galveston, Microbiology and Immuology, Galveston, Texas, United States.
Exposure to influenza A virus (IAV), respiratory syncytial virus (RSV), and human metapneumovirus (hMPV) is well-known to increase the risk of pneumonia in humans. Type I interferon (IFN-I) is a hallmark response to acute viral infections, and alveolar macrophages (AMs) constitute the first line of airway defense against opportunistic bacteria. Our study reveals that virus-induced IFN-I receptor (IFNAR1) signaling directly impairs AM-dependent antibacterial protection.
View Article and Find Full Text PDFAnn Am Thorac Soc
January 2025
Hangzhou Medical College, Hangzhou, China;
Rationale: Tobacco smoking is a well-established risk factor for idiopathic pulmonary fibrosis (IPF), yet the influence of early-life tobacco exposure on future IPF risk remains poorly understood.
Objectives: To test the hypothesis that early-life tobacco exposure may elevate the risk of developing IPF, with this effect potentially modified by genetic susceptibility to IPF and mediated through accelerated biological aging.
Methods: Using data from over 430,000 participants in the UK Biobank, we performed a prospective cohort study to examine the associations of maternal smoking around birth and age of smoking initiation with IPF risk.
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