A Review of Lead (Pb) and Cadmium (Cd) Contamination in Food Crops in Kenya

Main Article Content

Mary Rono Tanui

Keywords

Lead, cadmium, food safety, contamination, public health policy, Kenya

Abstract

In Kenya, rapid urbanization, poorly managed industrialization, and the intensive use of agrochemicals have heightened the risk of toxic element accumulation in the food supply chain. Among these contaminants, Lead (Pb) and Cadmium (Cd) pose severe risks due to their non-biodegradable nature, long biological half-lives, and high toxicity even at low concentrations. This study aimed to systematically synthesize a decade of empirical evidence (2016–2026) regarding lead (Pb) and cadmium (Cd) contamination in food crops in Kenya, map their geographic and anthropogenic pathways, characterize the associated multi-systemic human health risks, and identify structural regulatory gaps. Following a predefined systematic protocol, a narrative review was executed across major electronic databases (including PubMed, ScienceDirect, Scopus, Web of Science, Google Scholar, and AJOL). A total of 33 datasets for Pb and 14 for Cd evaluating concentrations in edible plant tissues, agricultural soils, and irrigation networks within Kenya were extracted and cataloged. Empirical data were stratified across urban, riverine, mining, commercial, and post-harvest retail zones, and benchmarked against international health thresholds established by the FAO, WHO, and Codex Alimentarius. The evidence revealed a stark, structurally entrenched contamination gradient following an urban-industrial > peri-urban riverine > rural high-input > rural low-input pattern. Leafy vegetables (kale, spinach, and indigenous greens) hyperaccumulated both metals. In the Nairobi-Machakos-Kiambu corridor, mean Pb concentrations in urban kale reached 0.68 ppm, driven by vehicular emissions, road dust, and untreated wastewater irrigation. Riverine systems like the Athi and Kabuthi river basins recorded extreme dry-season Pb concentrations up to 12.10 mg/kg due to industrial effluent. The most catastrophic localized exposure occurred in Migori County’s artisanal gold mining zones, where vegetable Pb levels climbed to 71.28 mg/kg (nearly 240 times the Codex limit) and soil Pb reached 706 mg/kg. Conversely, commercial farmlands in Trans Nzoia and Western Kenya exhibited systemic Cd soil enrichment exceeding WHO agricultural limits tenfold driven by the continuous application of phosphate-based fertilizers. Toxicological benchmarking indicated severe, multi-systemic, and intergenerational risks. Approximately 69% of children consuming Nairobi's urban-grown greens exceed daily Pb reference doses, predisposing them to irreversible neurodevelopmental injury, cognitive deficits, and downward social mobility. In adults, dietary Pb directly amplifies cardiovascular disease and mortality risks. Due to its 25-to-30-year biological half-life, cumulative dietary Cd exposure presents a silent epidemic of progressive renal tubular dysfunction, chronic kidney disease, bone demineralization, and multi-organ carcinogenicity via mutagenic and heritable epigenetic pathways. Kenya's food safety governance framework is currently inadequate, it lacks enforceable domestic maximum residue limits (MRLs), a national food contaminant surveillance program and sufficient laboratory infrastructure requiring urgent, coordinated, and evidence-based legislative and environmental interventions to safeguard Kenyan public health and food security

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