This review synthesizes evidence on aluminum exposure in infants and young children, emphasizing early life as a high-risk window for accumulation and toxicity. Clinically relevant exposure can occur via parenteral nutrition in premature or medically fragile infants, infant formula and complementary foods, drinking water chemistry, and aluminum-containing pharmaceuticals and adjuvants. Because renal clearance is developmentally limited and circulating aluminum is largely protein-bound, sustained exposure can promote tissue retention. Human clinical and observational data associate higher aluminum burden with poorer neurodevelopmental scores and with multisystem effects including impaired bone mineralization and hematopoietic disruption. The review also integrates emerging multi-omics findings linking prenatal trace element exposure, including aluminum, to shifts in infant gut microbiome composition and broad metabolomic remodeling, with potential implications for immune and neurodevelopmental programming. Regulatory controls and prevention priorities are discussed, with emphasis on minimizing exposure in high-risk settings and strengthening monitoring and manufacturing practices.
Aluminum exposure; infants; neurodevelopment; parenteral nutrition; infant formula; renal immaturity; bone mineralization; gut microbiome; metabolomics.
Aluminum is one of the most abundant elements in the earth’s crust and is ubiquitously present in the environment, making exposure inevitable for infants and young children [1]. However, aluminum has no known biological function and is considered a contaminant in most foods and medications [1]. The primary routes of aluminum exposure in infants differ significantly from those in older children and adults, with parenteral nutrition representing the most clinically significant source in premature and medically fragile infants.
Total parenteral nutrition (TPN) has historically been the most problematic source of aluminum exposure in hospitalized infants. A prospective study on premature infants receiving TPN found that aluminum levels increased significantly from cord blood (3.35 ± 1.73 µg/L) to day 14 of life (4.79 ± 3.54 µg/L), representing a statistically significant increase [2]. The increase was particularly associated with the duration of parenteral feeding, with infants receiving parenteral nutrition for more than 10 days showing significantly higher serum aluminum levels [2]. This concern has been documented extensively, with aluminum contamination in large-volume and small-volume parenterals, including calcium phosphate salts, albumin, and heparin, identified as major contributors to total aluminum burden [3].
Dietary exposure through infant formulas and complementary foods represents another significant exposure pathway. A risk assessment study from Lebanon analyzing 41 infant formula samples and 76 baby food products found average daily aluminum intake of 0.01–0.0104 mg/kg body weight per day for infants aged 0–23 months [4]. While individual food items contained aluminum below the limit of detection in many cases, the hazard quotient exceeded 1 for some male and female infants, suggesting potential health risks from cumulative dietary exposure [4]. A comprehensive Monte Carlo simulation approach for Iranian infant formulas and complementary foods revealed that aluminum concentrations significantly exceeded FAO/WHO standards in 80 formula milk and 27 baby food samples, with non-cancer hazard indices exceeding the safety threshold of 1.0 for all age groups [5].
Drinking water and environmental contamination contribute additional exposure pathways. While aluminum levels in drinking water are variable globally, the chemistry and bioavailability of aluminum are highly dependent on water pH and the specific chemical form present [6]. Children engaging in certain behaviors such as geophagy (soil ingestion) may receive substantially higher aluminum exposure, though this remains an underappreciated route of exposure in many populations.
Vaccine adjuvants containing aluminum have been the subject of considerable debate regarding pediatric safety. Aluminum salts serve as widely-used adjuvants in preventive vaccines and allergy immunotherapy preparations [7]. However, the clinical significance of this exposure route in relation to total aluminum burden remains controversial, though multiple studies have documented that the benefits of vaccination substantially outweigh potential aluminum adjuvant concerns [1].
The unique physiological characteristics of infants and young children render them particularly vulnerable to aluminum accumulation and toxicity. Unlike in older children and adults, the immature renal system of infants is unable to efficiently excrete absorbed aluminum, leading to preferential bioaccumulation in vulnerable tissues.
Aluminum absorption and tissue distribution patterns in infants differ markedly from adults. Preterm infants receiving parenteral aluminum face particular risk because the aluminum bypasses the gastrointestinal barrier entirely, and approximately 95% of circulating aluminum becomes bound to plasma proteins, chiefly transferrin [3]. However, approximately 5% remains ultrafilterable and is available for renal excretion. The developmental immaturity of the neonatal kidney presents a critical bottleneck, as glomerular filtration rates in preterm infants do not reach maturity until 34 weeks of gestation [3]. This physiological vulnerability means preterm infants have an additional burden to excrete the aluminum load they receive, which in many cases exceeds their renal capacity.
A comprehensive metallomics study examining 77 infant-mother pairs found remarkable disparities in metal burden between infants and their mothers. The geometric mean concentrations of lead, cadmium, and aluminum in infants were approximately three times higher than in their mothers (p < 0.0001), with some individuals showing burden levels several tens of times higher than their mothers [8]. This finding underscores the exceptional capacity of the infant body to accumulate these toxic metals relative to maternal exposure. Interestingly, the same study found that essential metal levels such as zinc, magnesium, and calcium in infants were significantly lower than in mothers, with 37.7% of child subjects estimated to be zinc-deficient [8]. Significant inverse correlations were observed between zinc and lead (r = 0.267, p = 0.019), and between magnesium and arsenic (r = 0.514, p < 0.0001), suggesting potential competitive absorption or transport mechanisms [8].
Clinical evidence of aluminum’s renal handling in infants comes from a notable case where an infant receiving high-aluminum parenteral solutions developed hypocalcemia when deferoxamine (an iron chelator with some aluminum-binding capability) was administered [3]. This case demonstrated the presumed sequence of events wherein aluminum interfered with calcium uptake in bone, resulting in osteopenia that took up the slack at the expense of serum calcium, a situation analogous to the “hungry bone syndrome” observed in primary hyperparathyroidism [3].
The metallomics field has enabled more sophisticated assessment of trace metal burden in infants. Recent work emphasizes that early assessment and intervention are crucial, as the toxic metal burden levels in infants and children warrant serious concern from the perspective of their harmful effects on normal growth and development [8]. The relationships between maternal and infant metal burdens vary by element, with aluminum showing a less intimate correlation with maternal exposure (r = 0.451) compared to mercury (r = 0.539), suggesting distinct absorption and retention mechanisms [8].
Aluminum’s neurotoxic properties represent one of the most clinically significant concerns in infant and child health. The developing brain undergoes critical periods of cell proliferation, migration, differentiation, and myelination during infancy and early childhood, making this period particularly vulnerable to neurotoxic insults.
Prenatal and early postnatal aluminum exposure has been associated with impaired neurodevelopment assessed via standardized developmental indices. A prospective cohort study examining prenatal metal exposure in the Wuhan Healthy Baby Cohort (N=1,088) found that higher maternal urinary levels of aluminum were significantly associated with lower Mental Development Index (MDI) scores in 2-year-old children [9]. The weighted quantile sum index of the metal mixture showed a significant inverse association with both MDI and psychomotor development index (PDI) scores, with aluminum contributing the most to the associations [9]. Interestingly, histidine, beta-alanine, purine, and pyrimidine metabolism significantly mediated these associations, suggesting that disturbances in amino acid, neurotransmitter, and neuroendocrine metabolism may be important mediators in contributing to impaired neurodevelopment of children [9].
The landmark clinical trial demonstrating aluminum’s neurotoxic effects involved preterm infants who received parenteral solutions containing high aluminum concentrations (45 µg/kg per day) compared to age-matched controls receiving low-aluminum solutions (4–5 µg/kg per day) [3]. The infants receiving high aluminum had significantly lower Bayley Mental Development Index scores at 18 months (92 ± 20 standard deviation) compared to those receiving low aluminum (102 ± 17). Among 157 infants without neuromotor impairment, exposure longer than 10 days resulted in a higher fraction of high-aluminum group having mental development index values below 85 points (38% versus 17%, p = 0.03) [3].
The mechanisms of aluminum neurotoxicity involve multiple pathways including oxidative stress, alterations in neurotransmitter systems, and disruption of calcium signaling. Aluminum is known to have neurotoxic properties that may induce clinical symptoms through oxidative stress and pro-inflammatory effects [2]. The element has been implicated in amyloidogenesis and other pathological processes relevant to neurodegenerative disease, though the specific mechanisms in developing versus mature brains remain incompletely understood [10].
Developmental vulnerability as a modifying factor in aluminum-related neurologic effects requires particular consideration. A comprehensive review examining exposure to mercury and aluminum in early life emphasized that the safety levels of these substances have never been properly determined for fetuses, newborns, infants, and children, despite their long use as active agents in medicines and fungicides [11]. The review concluded that neurobehavioral effects of aluminum-containing adjuvants are not extraordinary and are easily detected in both high and low-income countries, particularly when co-exposure to other neurotoxicants occurs [11].
Beyond neurotoxicity, aluminum’s effects on bone and mineral metabolism represent critical toxicological concerns in growing children. Aluminum-induced osteomalacia and bone disease were first recognized in uremic patients on dialysis but have subsequently been documented in non-uremic children receiving high-dose aluminum exposure through parenteral nutrition or other sources.
The characteristic bone pathology associated with chronic aluminum exposure includes defective mineralization at the bone-forming surface, where aluminum accumulates [3]. Histochemical staining in biopsy specimens reveals aluminum deposition at the mineralization front, identical to the site where new bone forms. Dynamic histomorphometric analyses of biopsies from patients receiving long-term aluminum-containing TPN produced a striking finding: the quantitative concentration of aluminum at the mineralization front inversely correlated with the rate of bone formation [3]. Substitution of deionized water for dialysate use and the introduction of non-aluminum-containing phosphate-binding gels and crystalline amino acids led to gradual resolution of bone pain and improved bone formation [3].
Aluminum toxicity-induced disease manifestations in children include vitamin D-resistant osteomalacia characterized by deranged membranous bone formation, accumulation of osteoid matrix, reduced mineralization, decreased numbers of osteoblasts and osteoclasts, and decreased lamellar bands with elevated aluminum concentrations [6]. This disease can progress to stress fractures of the ribs, femur, vertebrae, humerus, and metatarsals. Serum aluminum concentrations exceeding 100 µg/L have been reported with 75–88% positive predictive value for aluminum bone disease [6].
Chronic aluminum exposure also manifests through hematopoietic effects, including an erythropoietin-resistant microcytic hypochromic anemia [6]. This anemia likely reflects aluminum’s interference with iron metabolism and heme synthesis pathways. The metallomics study mentioned previously documented that essential metal levels such as zinc, magnesium, and calcium in infants were significantly lower than in mothers [8], suggesting that aluminum may competitively interfere with the absorption or retention of essential minerals critical for normal growth, bone development, and hematopoiesis.
Central nervous system manifestations of chronic aluminum exposure include speech difficulty, mutism, facial grimacing, multifocal seizures, and dyspraxia, related to aluminum accumulation in the brain [6]. These neurologic manifestations may progress to frank encephalopathy in severe cases, emphasizing the multisystem nature of aluminum toxicity.
The emerging field of microbial metallomics has revealed previously unrecognized interactions between aluminum exposure and the developing infant microbiome. These interactions occur during a critical window of microbiome colonization and maturation and may have long-term consequences for immune development and metabolic health.
A landmark multi-omics study examining 146 mother-infant pairs found that prenatal trace element exposure, including aluminum, significantly impacts the developing infant gut microbiome [12]. The study measured trace elements in maternal hair samples and collected stool samples from infants at 3, 6, and 12 months after delivery for amplicon sequencing, metagenomics, and metabolomics. Results demonstrated that relative abundance of Bifidobacterium—a keystone genus associated with healthy infant development—increases under high exposure to aluminum and manganese [12]. During the first year of life, infants and their paired mothers had distinct microbial diversity and composition, with their bacterial community structures gradually approaching each other over time [12]. The study identified 56 differential metabolites between the first and second visit and 515 differential metabolites between the second and third visit, indicating substantial metabolome remodeling associated with prenatal metal exposure [12].
The differential impact of specific trace elements on infant microbiota composition was precisely quantified. Shannon diversity in 3-month-old infants was correlated positively with selenium and negatively with copper, demonstrating element-specific effects on microbial diversity [12]. Importantly, the study revealed that high levels of copper and arsenic exposure may induce the enrichment of antibiotic resistance genes (ARGs) in the infant gut, a finding with potential long-term implications for antimicrobial resistance [12].
Microbial metallomics analysis has identified aluminum-tolerant microbial populations that colonize infant-associated microbiota. An innovative artificial intelligence-assisted Raman-activated cell sorting (AI-RACS) system was used to identify and characterize aluminum-tolerant microbes from environmental samples, validating the capacity of this technology to segregate microbial cells from intricate environmental samples and investigate their functional attributes [13]. This technological advance has enabled identification of specific bacterial strains capable of thriving under aluminum stress conditions, an important consideration for understanding the adaptive responses of infant microbiota.
The mechanisms by which microorganisms tolerate and respond to aluminum exposure involve sophisticated metalloproteins and regulatory systems. Heavy metal tolerance in bacteria includes the formation of biofilms, efflux systems, and enzymatic detoxification pathways that allow communities to adapt and survive in contaminated environments [14]. These adaptations are enhanced by mutations in genes and horizontal gene transfer, enabling microbial species to survive stress while simultaneously contributing to nutrient cycling and decomposition of organic matter [14]. Plant growth-promoting rhizobacteria such as Rhizobium and Bacillus are known contributors to phytoremediation processes and have demonstrated metal-binding capabilities and biosorption applications [14].
The metabolomics alterations observed in aluminum-exposed infant microbiota reflect the metabolic burden imposed by metal stress. Beyond simple compositional shifts, aluminum exposure triggers coordinated changes in microbial metabolite production, including differential expression of metabolic pathways involved in stress responses. The identification of 515 differential metabolites between sequential visits in aluminum-exposed infants suggests substantial rewiring of metabolic networks, potentially affecting nutrient bioavailability, immune stimulation, and neurodevelopmental pathways that depend on bacterial metabolite production [12].
Microbial metallomics assessment in infants has utilized mass spectrometry-based approaches to characterize metallophore production—specialized metal-chelating compounds produced by pathogenic and commensal microorganisms during infection and colonization stress [15]. These metallophores represent sensitive, noninvasive biomarkers of microbial metabolic state and may indicate shifts in microbiota composition and function in response to aluminum and other metal stress [15].
Recognition of aluminum’s toxicological potential in infants and children has led to regulatory interventions, though the adequacy and implementation of these standards remain subjects of ongoing scientific debate and refinement.
The United States Food and Drug Administration has been investigating aluminum contamination in parenteral solutions since 1986, ultimately proposing regulations to limit aluminum contamination and require labeling of products containing aluminum [3]. The regulatory response specifically addressed the concern that continuous delivery of high aluminum loads could confer cumulative toxicity, particularly in neonates receiving large infusions of aluminum-containing solutions. The FDA proposed amending regulations to add labeling requirements concerning aluminum and to specify an upper limit of 25 µg/L for certain large-volume parenteral solutions such as sodium chloride, dextrose, and water [3]. For small-volume components and biologicals, the FDA required applicants to submit approval with validated assay methods and to state the product’s aluminum content and its concentration at the expiry date on immediate container labels and pharmacy bulk packages [3].
Despite these regulatory efforts, total aluminum concentration from some components continues to exceed the recommended final concentration in parenteral solutions [1]. The North American Society for Pediatric Gastroenterology and Nutrition responded to the FDA proposed rule by strongly endorsing interest in safety and encouraging expanded activity in restricting aluminum in biological agents, particularly albumin and other colloidal volume expanders [3]. The organization emphasized the need for specific definitions that would closely guide compounds administered to infants, given that no universally accepted safe daily aluminum dose has been established [3].
Dietary standards for aluminum have been established by international organizations. The provisional tolerable weekly intake (PTWI) set by JECFA is less than 6–7% of total complementary intake for both female and male infants aged 0–23 months, based on a tolerable intake of 2 mg/kg body weight per week [4]. However, in some populations consuming aluminum-contaminated water or foods, the hazard quotient has been estimated to exceed 1, indicating potential non-cancer health risks [4].
The clinical management of aluminum toxicity in infants and children remains challenging. Chelation therapy using deferoxamine has been attempted in some cases but carries its own risks and is not routinely recommended for pediatric aluminum toxicity unless there is evidence of serious organ involvement. Instead, the primary focus remains on prevention through reduction of exposure, particularly in vulnerable populations such as preterm infants receiving parenteral nutrition, infants in regions with high-aluminum drinking water, and those consuming contaminated complementary foods.
Prevention strategies and exposure reduction represent the most practical approach. In clinical settings, measures to reduce aluminum exposure include substituting deionized water for dialysate use, implementing non-aluminum-containing phosphate-binding gels when necessary, using crystalline amino acids instead of casein hydrolysate in parenteral solutions, and adhering to validated manufacturing standards for large- and small-volume parenterals [3]. For infants and young children in home settings, awareness of potential aluminum contamination in drinking water and food sources, along with selection of infant formulas from manufacturers implementing quality control measures to minimize aluminum content, represents important preventive strategies.
The concerns about aluminum in infant formulas and antiperspirants have not been substantiated by robust evidence, though they warrant continued research [1]. In contrast, the evidence linking long-term, high-concentration aluminum exposure to neurodevelopmental impairment, bone disease, and microbiome alterations is substantial and warrants serious attention from healthcare providers and public health authorities.
Future research needs include larger epidemiological and intervention studies to clarify the thresholds for developmental toxicity in diverse populations, longitudinal assessments of microbiome recovery following cessation of high aluminum exposure, mechanistic studies of aluminum-microbiota interactions and their long-term health consequences, and development of biomarkers that can identify infants at greatest risk of aluminum-related adverse effects. The integration of metallomics, microbiomics, and metabolomics approaches—termed “multi-omics”—offers particular promise for understanding the complex interactions between aluminum exposure, microbiota composition, and developmental health outcomes [12].
The unique vulnerability of infants and young children to aluminum toxicity demands continued vigilance and scientifically-informed public health measures. As the field advances, understanding the mechanisms linking aluminum exposure, microbiome dysbiosis, and developmental impairment may lead to novel preventive and therapeutic interventions protecting the health of the world’s most vulnerable populations.
A central implication of the evidence reviewed is that aluminum risk in early life is determined less by the ubiquity of background exposure and more by the intersection of developmental physiology with concentrated, sustained inputs. Infants, and particularly preterm infants, possess an intrinsic toxicokinetic disadvantage because renal clearance is immature. In the context of medically administered aluminum, this creates a predictable scenario in which aluminum delivery can outpace excretory capacity, enabling bioaccumulation during a period of rapid neurodevelopment and skeletal mineralization. The review’s emphasis on protein binding also reinforces why relatively small ultrafilterable fractions can still matter clinically when exposure is continuous and renal function is constrained.
The neurodevelopmental signal is supported by convergent clinical and epidemiologic findings that are directionally consistent. The preterm parenteral nutrition trial provides a particularly instructive anchor because it links a defined exposure contrast to an interpretable developmental endpoint, with lower Bayley Mental Development Index scores in the higher-aluminum group and a higher proportion of infants below a clinically relevant threshold after prolonged exposure. In parallel, a prospective cohort analysis associating higher prenatal aluminum exposure with lower Mental Development Index scores at age two, including evidence that aluminum contributed materially within a mixture framework, suggests that clinically relevant effects may not be confined to intensive care settings. The reported mediation by histidine, beta-alanine, purine, and pyrimidine pathways further supports biological plausibility by implicating metabolic perturbations that can map onto neurotransmitter, neuroendocrine, and developmental processes.
Bone and mineral metabolism outcomes expand the interpretive frame beyond “neurotoxicity” and highlight aluminum as a systemic developmental toxicant when exposure is sustained. The described pathology of defective mineralization at the bone-forming surface, with aluminum deposition at the mineralization front and an inverse relationship between aluminum burden and bone formation rate, is mechanistically coherent with growth-period vulnerability. The clinical account in which aluminum exposure plausibly interfered with calcium uptake in bone, leading to osteopenic dynamics with downstream hypocalcemia, underscores that these effects can be clinically consequential rather than merely histologic.
The review also points toward an underappreciated dimension of aluminum exposure: its capacity to shape the developing gut ecosystem and metabolite milieu during the first year of life. Multi-omics data from mother–infant pairs indicate that prenatal heavy metal exposure, including aluminum, is associated with measurable changes in infant gut microbiome composition and substantial longitudinal remodeling of the metabolome across infancy. Although the reported increase in Bifidobacterium under higher aluminum and manganese exposure could be interpreted as benign or even favorable in isolation, compositional directionality is not sufficient to infer health impact. The more actionable signal is functional: large-scale metabolomic shifts suggest coordinated rewiring of microbial and host metabolic networks under metal stress, with plausible implications for nutrient bioavailability, immune stimulation, and neurodevelopmentally relevant microbial metabolite production. The discussion of aluminum-tolerant microbial populations and known bacterial heavy metal tolerance strategies (biofilms, efflux, detoxification, and horizontal gene transfer) further reinforces that metals can act as ecological selectors, potentially altering resilience, stability, and downstream host exposures through microbiome-mediated mechanisms.
From a risk characterization standpoint, several interpretive cautions remain essential. First, “aluminum” is not a single exposure entity; bioavailability depends on chemical form and context, as highlighted for drinking water, where pH and speciation influence biological behavior. Second, early-life exposure frequently occurs as a mixture, and mixture modeling suggests that aluminum may act within broader co-exposure patterns, complicating attempts to assign risk to a single metal without considering correlated contaminants and shared sources. Third, biomarkers can be imperfect. Serum aluminum thresholds have been used in specific contexts. Still, serum measures may not reliably reflect cumulative tissue deposition or timing of exposure, particularly when exposure is intermittent or when distributional kinetics differ across compartments. These limitations strengthen the rationale for prevention-oriented governance rather than reliance on late-stage clinical detection.
The regulatory discussion in the review supports a practical conclusion: the highest-yield risk-reduction opportunities exist where aluminum exposure is both avoidable and concentrated, namely in parenteral products and in selected high-exposure dietary contexts. The FDA’s longstanding focus on limiting aluminum contamination and requiring labeling for parenteral solutions recognizes that continuous delivery in neonates can create cumulative toxicity risk. The persistence of components exceeding recommended concentrations indicates that implementation gaps and supply constraints remain relevant, and that procurement and compounding practices can meaningfully influence infant exposure in clinical settings. For dietary exposure, risk assessments of infant formulas and young-child foods suggest that some populations may exceed non-cancer risk thresholds when cumulative intake is considered, reinforcing the need for manufacturing controls, source selection, and surveillance tailored to infant consumption patterns.
Finally, the review’s forward-looking recommendations align with a coherent research agenda. Priority areas include larger epidemiologic studies to clarify developmental toxicity thresholds across diverse settings, longitudinal tracking of microbiome and metabolome recovery after exposure reduction, mechanistic studies of aluminum–microbiota interactions, and biomarker development to identify infants at greatest risk. Importantly, the integration of microbiomics and metabolomics is not merely descriptive; it offers a path toward causal inference by linking exposure to functional intermediates that can plausibly mediate neurodevelopmental and immunometabolic outcomes.
In aggregate, the evidence supports a defensible clinical and public health posture: sustained, higher-intensity aluminum exposures in early life warrant serious attention, particularly where renal immaturity and continuous administration amplify retention risk, and where ecological selection pressures on the gut microbiome may translate metal exposure into broader developmental programming effects.
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