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BackgroundTobacco smoke may affect atopic dermatitis (AD) because of its known effects on humoral and cellular immunity, but prior studies lack data on disease severity and biomarkers over time.ObjectiveWe investigated the association between passive and active tobacco smoke exposure (TSE) during childhood and adolescence and the activity and severity of AD.MethodsA birth cohort of 10,521 individuals was followed through adolescence as part of the Avon Longitudinal Study of Parents and Children. We used mixed-effect models to determine the risk of AD (based on repeated assessments) with passive smoke exposure during childhood, active TSE during adolescence, and using a serum biomarker of tobacco exposure (cotinine) at 3 time points.ResultsAfter adjusting for confounding factors, there was no evidence of a relationship between passive TSE and concurrent AD activity in childhood (adjusted odds ratio, 0.95; 95% confidence interval, 0.83, 1.07) or of an increased risk between active smoking and AD activity in adolescence (adjusted odds ratio, 0.57; 95% confidence interval, 0.44, 0.75). Secondary analyses demonstrated no dose-response relationship and no increased severity of AD with passive or active TSE. Furthermore, we found no increased risk of AD with a cumulative measure of passive TSE across childhood (adjusted relative risk ratio, 0.98; 95% confidence interval, 0.96, 1.00).ConclusionNeither active nor passive TSE was associated with AD during childhood and adolescence.

BackgroundAtopic dermatitis is known to be common among children, but there are few studies examining the epidemiology across the life course. In particular, there is a paucity of data on atopic dermatitis among older adults.ObjectiveTo evaluate participant characteristics, patterns of disease activity and severity, and calendar trends in older adult atopic dermatitis in comparison to other age groups in a large population-based cohort.MethodsThis was a cohort study of 9,154,936 individuals aged 0-99 years registered in The Health Improvement Network, a database comprised of electronic health records from general practices in the United Kingdom between 1994 and 2013. Atopic dermatitis was defined by a previously validated algorithm using a combination of at least one recorded atopic dermatitis diagnostic code in primary care and two atopic dermatitis therapies recorded on separate days. Cross-sectional analyses of disease prevalence were conducted at each age. Logistic mixed effect regression models were used to identify predictors of prevalent disease over time among children (0-17 years), adults (18-74 years), and older adults (75-99 years).ResultsPhysician-diagnosed atopic dermatitis was identified in 894,454 individuals with the following proportions in each age group: 18.3% of children, 7.7% of adults, and 11.6% of older adults. Additionally, atopic dermatitis prevalence increased across the 2-decade period (beta from linear regression test for trend in the change in proportion per year = 0.005, p = 0.044). In older adults, atopic dermatitis was 27% less common among females (adjusted OR 0.73, 95% CI 0.70-0.76) and was more likely to be active (59.7%, 95% CI 59.5-59.9%) and of higher severity (mean annual percentage with moderate and severe disease: 31.8% and 3.0%, respectively) than in other age groups.ConclusionIn a large population-based cohort, the prevalence of physician-diagnosed atopic dermatitis has increased throughout adulthood and was most common among males age 75 years and above. Compared to children ages 0-17 and adults ages 18-74, older adult atopic dermatitis was more active and severe. Because the prevalence of atopic dermatitis among older adults has increased over time, additional characterization of disease triggers and mechanisms and targeted treatment recommendations are needed for this population.

Purpose of reviewThis theoretical review identifies physiological mechanisms by which violence against women (VAW) may increase women's susceptibility to HIV through trauma, stress, and immune dysfunction.Recent findingsResearch documents systemic and local immune responses are related to stress and trauma from abuse across the life course (i.e., childhood, IPV, adulthood re-victimization). Findings are interpreted within a theoretical framework grounded in the Social Stress Theory and the concept of toxic stress, and highlight the current state of the science connecting: (1) VAW to the physiological stress response and immune dysfunction, and (2) the physiological stress response and inflammation to HIV susceptibility and infection in the female reproductive tract. Despite a dearth of research in human subjects, evidence suggests that VAW plays a significant role in creating a physiological environment conducive to HIV infection. We conclude with a discussion of promising future steps for this line of research.

Background: Tobacco smoke may affect atopic dermatitis (AD) because of its known effects on humoral and cellular immunity, but prior studies lack data on disease severity and biomarkers over time., Objective: We investigated the association between passive and active tobacco smoke exposure (TSE) during childhood and adolescence and the activity and severity of AD., Methods: A birth cohort of 10,521 individuals was followed through adolescence as part of the Avon Longitudinal Study of Parents and Children. We used mixed-effect models to determine the risk of AD (based on repeated assessments) with passive smoke exposure during childhood, active TSE during adolescence, and using a serum biomarker of tobacco exposure (cotinine) at 3 time points., Results: After adjusting for confounding factors, there was no evidence of a relationship between passive TSE and concurrent AD activity in childhood (adjusted odds ratio, 0.95; 95% confidence interval, 0.83, 1.07) or of an increased risk between active smoking and AD activity in adolescence (adjusted odds ratio, 0.57; 95% confidence interval, 0.44, 0.75). Secondary analyses demonstrated no dose-response relationship and no increased severity of AD with passive or active TSE. Furthermore, we found no increased risk of AD with a cumulative measure of passive TSE across childhood (adjusted relative risk ratio, 0.98; 95% confidence interval, 0.96, 1.00)., Conclusion: Neither active nor passive TSE was associated with AD during childhood and adolescence., Competing Interests: Funded by National Institutes of Health grants via Arthritis and Musculoskeletal and Skin Diseases Career Development Award K23AR073915 (to K.A.), National Center for Advancing Translational Sciences award UCSF-CTSI grant UL1 TR001872 (to C.E.M.), and UCSF-CTSI grant TL1TR001871 (to F.R.). Funding was also received from a Wellcome Trust Senior Research Fellowship in Clinical Science (award 205039/Z/16/Z to S.M.L.); and from the UCSF Summer Explore Fellowship (to N.A.A. and L.N.C.). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the report. The findings and conclusions in this report are those of the authors and do not necessarily represent the views of the funders. The UK Medical Research Council and Wellcome (grant 217065/Z/19/Z) and the University of Bristol provide core support for ALSPAC. This publication is the work of the authors and will serve as guarantors for its contents. A comprehensive list of grant funding is available on the ALSPAC website (www.bristol.ac.uk/alspac/external/documents/grant-acknowledgements.pdf). Disclosure of potential conflict of interest: K. Abuabara reports receipt of consulting fees from TARGET RWE and grants to her institution from Pfizer and Cosmetique International SNC. The rest of the authors declare that they have no relevant conflicts of interest., (© 2024 The Authors.)