Introduction:

Exposure to xenobiotics from the environment and occupational settings, and the attendant associated expression of neurological disorders (NDs), is a major and fast growing emerging global health burden. Globally, an estimation of over 3.4 billion persons (43.1% of the global population), suffers at least an ND, and this is increasing annually. World Health Organization raised concern towards understanding the etiologies associated with NDs, as search for a lasting remedy. Xenobiotics (metals, organic pollutants particulate matters, microorganisms, and radiations), readily emitted from inappropriate solid waste (SW) management, are increasingly recognized as important risk factors in ND expression. This study aimed to determine the mechanisms linking exposure to mixture of contaminants from SWs to expressions of neurological disorders in human.

Methodology:

This study utilized a qualitative and quantitative analyses of secondary data obtained using standard eligibility criterion in accordance with Preferred Reporting Items for Systematic Reviews and Meta- Analysis (PRISMA) framework. Data were analyzed using inferential statistics, data visualization and meta-analysis of standardized mean difference (SMD) to measure the effect size.

Results and discussion:

Exposure to xenobiotics emitted from SW significantly increased multiple ND outcomes at varying frequencies: fetal and child neurodevelopment impairment, cognitive deficits, stroke, asthma, allergies, and attention-deficit/hyperactivity disorder. The mechanisms of ND expressions induced by SW emitted xenobiotics (metals, organic compounds and particulate matters) include disruption of neuronal integrity, alterations in neurotransmitter systems, induction of oxidative stress and enzyme dysregulation, neuroinflammation and epigenetic modifications (particularly DNA methylation of genes involved in brain development). Meta-analysis of ND biomarker assessments revealed significant positive effect sizes for neurological biomarkers (p ≤ 0.0001). This indicates increased risk of ND expressions among environmentally and occupationally exposed populations, despite substantial heterogeneity (I² = 94.88%). Conclusively, SW-derived xenobiotics are poorly studied source of NDs in humans, despite being an emerging area of environmental public health. Regulation of indiscriminate SW disposal and prevention of exposure to xenobiotic emission from SW may significantly reduce NDs in exposed populations.