Association Between Solid-Fuel Household Air Pollution and Systemic Inflammatory Biomarkers in Adults: A Systematic Review

Background Roughly one-third of the world's population still relies on solid fuels (wood, crop residue, dung, coal, charcoal) for cooking and heating, generating household air pollution (HAP) that was linked to an estimated 2.31 million deaths globally in 2019. Systemic inflammation is a proposed intermediate pathway linking HAP exposure to cardiovascular, metabolic, and respiratory disease, but the magnitude and consistency of this association in adults has not been systematically synthesised. Objective To systematically review, and quantitatively synthesise evidence on the association between solid-fuel HAP exposure and circulating, blood-based (systemic) inflammatory biomarkers, principally C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), interleukin-8 (IL-8), and endothelial adhesion molecules among adults. Urinary, oxidative-stress, and other mechanistic or cardiometabolic markers were considered as secondary, supportive evidence only. Methods We conducted a structured literature search (PubMed/PMC, ScienceDirect, Wiley Online Library, SpringerLink, and PLOS, supplemented by citation chaining) for studies published in English reporting systemic inflammatory biomarker concentrations in adults exposed to solid-fuel HAP relative to a lower-exposure or clean-fuel comparator. Screening followed PRISMA 2020 principles. Given substantial heterogeneity in biomarker assays, exposure metrics, and reporting formats across studies, we conducted a structured narrative synthesis with a semi-quantitative harvest plot consistent with Synthesis Without Meta-analysis (SWiM) guidance. Risk of bias was assessed using an adapted Newcastle-Ottawa Scale for non-randomised studies. Results Nine studies met eligibility criteria (seven cross-sectional, one household-level cross-sectional multi-site study, one randomised controlled trial), conducted across India, China, Peru, Honduras, Nigeria, and South Africa. Combining the seven studies that reported a clear individual-level analytic sample size yields at least 2,362 adults; one further study enrolled 617 households rather than individually sampled adults, and one study's precise analytic sample size was not clearly stated in the available source material. Among the eight primary-tier studies, CRP was the most frequently reported biomarker (6 of 8) and was significantly elevated among solid-fuel-exposed adults in 4 studies, significantly lower in 1 study, and null in 1 study. IL-6 and TNF-α were each reported in 4–5 primary-tier studies, with most showing significant elevation among solid-fuel users. Two studies including the largest (n = 415) found no significant associations for most biomarkers, and one study reported an unexpected inverse association for CRP alongside elevated adhesion molecules in the same population. Conclusions The preponderance of available evidence supports an association between solid-fuel HAP exposure and higher systemic inflammatory biomarker levels in adults, most consistently for CRP, IL-6, and TNF-α, and this is biologically plausible given experimental and mechanistic data. However, the evidence base is small, geographically clustered, predominantly cross-sectional, and heterogeneous in exposure and outcome measurement, precluding a statistically pooled effect estimate at this time. Larger, standardised, longitudinal studies ideally nested within cookstove-intervention trials are needed to quantify this relationship precisely and to clarify its contribution to the cardiovascular and metabolic burden of HAP.