Author

W. Adikusuma

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Review Open access Sep 2026

Global, regional, and national prevalence of second-hand smoke and attributable disease burden in 204 countries and territories, 1990-2023: a systematic analysis for the Global Burden of Disease Study 2023.

BACKGROUND Second-hand smoke (SHS) exposure remains a major source of morbidity and mortality among non-smokers. This study presents the first dedicated Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) publication to systematically quantify SHS prevalence and evaluate its effect as a global risk factor across a broader range of outcomes. METHODS Using the GBD 2023 comparative risk assessment framework, we estimated SHS exposure prevalence and attributable disease burden across 204 countries and territories from 1990 to 2023, stratified by age and sex. Exposure estimates were derived by synthesising population-based surveys and household composition data through spatiotemporal Gaussian process regression. Relative risks for nine health outcomes, now including asthma, were estimated using the Burden of Proof methodology, and applied to calculate attributable deaths and disability-adjusted life-years (DALYs). FINDINGS In 2023, an estimated 2·71 billion (95% UI 2·44-3·02) people worldwide were exposed to SHS, including 767 million (687-858) children aged 0-14 years. Age-standardised prevalence was highest in southeast Asia, east Asia, and Oceania (48·4% [44·0-53·4]), with female individuals in some countries experiencing nearly 1·8 times the exposure prevalence of male individuals. Despite a 22·2% (10·6-32·4) decline in global age-standardised prevalence since 1990, this progress has not been sufficient to reduce the absolute number of exposed individuals, which has remained stable globally and has risen sharply in sub-Saharan Africa (98·5% [62·0-144·4] increase) and North Africa and the Middle East (72·1% [47·8-101·8] increase). In 2023, SHS exposure accounted for 1·66 million (1·33-2·07) deaths and 44·8 million (35·8-54·3) DALYs globally. Ischaemic heart disease was the leading contributor to SHS-attributable DALYs (12·0 million [9·31-15·2]) overall, while lower respiratory infections predominated among children (5·16 million [3·48-7·12]). INTERPRETATION We estimated that SHS remains a substantial driver of global health loss, particularly through cardiovascular and paediatric respiratory diseases. Persistent geographical disparities and growing absolute numbers of exposed individuals in several regions underscore the urgent need for accelerated implementation and enforcement of comprehensive tobacco control measures, particularly to protect women and children in both public and domestic environments. FUNDING Bloomberg Philanthropies and the Gates Foundation.

Luisa S. Flor, Jason A Anderson, Brooks W. Morgan et al. · Lancet Public Health · 0 citations

Open access Jul 2026

Integrative bioinformatics analysis identifies APOE as a candidate link between lipid dysregulation and macrophage activation in inborn errors of metabolism

Background Inborn errors of metabolism (IEM) are a heterogeneous group of genetic disorders characterized by metabolic dysregulation and high mortality. Despite extensive genetic discoveries, the molecular mechanisms underlying severe disease progression remain incompletely understood. Increasing evidence suggests that host metabolic states, particularly lipid dysregulation, can profoundly influence immune cell function and may contribute to impaired responses against intracellular pathogens. Methods We integrated genomic data from four high-confidence databases (GWAS Catalog, CTD, Open Targets, and ClinVar) and identified 1,288 IEM-associated genes. Disease ontology enrichment, multi-parametric functional annotation, and cell-type enrichment analyses were performed using Open-XGR, WebGestalt, and Tabula Sapiens. Bioinformatics findings were interpreted alongside clinical and cytomorphological observations from a pair of one-year-old twins with suspected IEM and macrophage activation syndrome. No patient-specific genetic or molecular validation of APOE was available. Results Functional annotation identified APOE as the highest-scoring gene across seven biological categories, with enrichment in lipid metabolism- and macrophage-related pathways. Cell-type enrichment demonstrated an overrepresentation of IEM-associated genes in macrophage-related reference signatures, including datasets annotated as M2 macrophages. APOE was the only gene consistently represented across macrophage, M2 macrophage, protein–lipid complex, and vasculature-associated macrophage categories. Clinical evaluation of the twin cases showed persistent hyperbilirubinemia, elevated transaminases, cholestasis, and macrophage activation. Bone marrow and cerebrospinal fluid cytology demonstrated lipid-laden monocyte/macrophage morphology. These clinical observations are concordant with lipid-handling abnormalities in macrophages but do not establish an APOE-dependent mechanism or macrophage polarization state. Conclusion This study identifies APOE as a highly prioritized candidate gene associated with lipid metabolism pathways and macrophage-related signatures in IEM. These findings support the hypothesis that APOE-associated lipid dysregulation may contribute to macrophage dysfunction and warrant further experimental validation.

Rahmat Dani Satria, Riswan Hadi Kusuma, Nazhipah Isnani et al. · Frontiers in Pharmacology · 0 citations