Glyphosate herbicide has been linked with airway diseases in adults. Evidence remains inconsistent, without investigations conducted in youthful populations. This study aims to examine the association between glyphosate and obstructive airway diseases in adult and youth samples in the National Health and Nutrition Examination Survey. Glyphosate exposure was categorized into tertiles. Separate multiple logistic regressions were conducted for adults and youths, adjusting for relevant covariates. Analyses were stratified by age. Sensitivity analyses explored associations with past-year asthma-related events. In total, 4031 adults and 1692 youths were included. There was a significant dose–response relationship between glyphosate and airway diseases in adults (tertile 2: aOR = 1.17, 95% UI: 0.94, 1.46, p = 0.15; tertile 3: aOR = 1.29, 95% UI: 1.02, 1.62, p = 0.03). Weak associations were shown between glyphosate and asthma in the youth sample (aOR = 1.08, 95% UI: 0.74, 1.58, p = 0.69); however, the relationship was more pronounced in adolescents (aOR = 1.33, 95% UI: 0.82, 2.15, p = 0.24). A dose–response pattern was observed between recent exposure and temporal outcomes in adults, reaching up to 75% higher odds of past-year asthma attacks among participants with glyphosate levels at the third tertile (tertile 3: aOR = 1.75, 95% UI: 0.92, 3.36, p = 0.09). These warrant timely monitoring and prevention strategies, with future research focusing on investigating longitudinal associations.

Background: Vitamin D is an important immunomodulator in host defense against Mycobacterium tuberculosis, yet most tuberculosis-related research has focused on the vitamin D receptor (VDR). The contribution of vitamin D metabolism genes, particularly cytochrome P450 (CYP) enzymes, remains less clearly defined. Methods: We conducted a narrative review examining the role of major vitamin D–metabolizing enzymes, including CYP2R1, CYP27A1, CYP27B1, and CYP24A1, in tuberculosis susceptibility, immune regulation, and treatment response, with additional focus on diabetes mellitus as a major comorbidity. Evidence from genetic association studies, observational studies, mechanistic experiments, and clinical data was synthesized. Results: Vitamin D metabolism enzymes influence intracellular vitamin D activation and inactivation, affecting antimicrobial peptide production, autophagy, cytokine signaling, and macrophage-mediated clearance of M. tuberculosis. Genetic and epigenetic variation in these pathways may contribute to differences in tuberculosis risk and prognosis. Diabetes mellitus may further disrupt these mechanisms through chronic hyperglycemia, oxidative stress, inflammation, impaired macrophage and T-cell function, and alterations in vitamin D metabolism, potentially increasing tuberculosis susceptibility and worsening outcomes. However, direct evidence for several enzymes remains limited. Inconsistent findings from vitamin D supplementation trials suggest that circulating 25(OH)D may not accurately reflect functional vitamin D activity at infection sites. Current evidence is largely mechanistic, observational, and genetic, with few interventional studies. Conclusion: Vitamin D metabolism genes represent an underexplored but potentially important component of tuberculosis pathophysiology, particularly in patients with diabetes. Future work should prioritize genetically stratified host-directed approaches to identify patients most likely to benefit from vitamin D–based interventions.

Per- and polyfluoroalkyl substances (PFAS) are environmentally persistent chemicals commonly employed in heat- and water-resistant applications. Experimental evidence indicates a biological plausibility for PFAS-related carcinogenic effects through mechanisms such as oxidative stress and immunomodulation; however, epidemiological evidence regarding skin cancers remains limited. This study aimed to investigate the association between serum concentrations of three understudied PFAS—perfluorodecanoic acid (PFDA), perfluoroundecanoic acid (PFUnDA), and 2-(N-methyl-perfluorooctane sulfonamido) acetic acid (2-(N-methyl-PFOSA) acetate)—and the incidence of non-melanoma skin cancer (NMSC) and melanoma among U.S. adults. We conducted a cross-sectional analysis utilizing data from eight NHANES cycles (2003–2018), which included 5,934 adults aged 20 years and older with complete data. Skin cancer outcomes were determined based on self-reported physician diagnoses, while PFAS concentrations were assessed in serum samples. We employed multivariable logistic regression, adjusting for age, sex, race/ethnicity, body mass index, smoking status, and NHANES cycle. PFAS exposure was evaluated using tertiles, detectable/undetectable status, and log-transformed continuous measures. Additionally, exploratory age- and sex-stratified analyses were conducted using Firth penalized logistic regression, and multiple imputation was applied to address potential selection bias due to missing covariates. Compared to the lowest tertile, PFDA in the second tertile was associated with an increased likelihood of NMSC (adjusted odds ratio [aOR] 1.73, 95% uncertainty interval [UI] 1.01–2.89; p=0.048), although no clear dose–response trend was observed across tertiles. Among adults aged 60 years and older, PFDA in the second tertile was linked to higher odds of NMSC (aOR 2.29, 95% UI 1.29–4.05; p=0.004). Associations for PFUnDA and 2-(N-methyl-PFOSA) acetate were generally inconsistent across exposure metrics, and analyses for melanoma did not reveal a definitive association. These findings suggest a potential link between higher PFDA exposure and NMSC, particularly in older adults, underscoring the necessity for ongoing PFAS monitoring and well-designed prospective studies to elucidate the temporal relationship and causality.