The Hidden Threat of Antimony: From Plastic Bottles to Cosmetics and Effective Detoxification Strategies

While public health discourse frequently focuses on well-known toxic metals such as lead, mercury, and arsenic, antimony—a metalloid element with properties similar to arsenic—remains a largely overlooked environmental and health concern. This relative obscurity is particularly troubling given antimony's widespread presence in modern consumer products, including polyethylene terephthalate (PET) plastic bottles, traditional cosmetics, flame retardants, and various industrial applications. Recent research has documented alarming levels of antimony leaching from plastic beverage containers, raising questions about chronic low-level exposure through one of the most ubiquitous materials in modern life (Shotyk & Krachler, 2007).

Antimony trioxide serves as a catalyst in PET production and a synergist in brominated flame retardants, while antimony sulfide has been used for millennia in traditional eye cosmetics across Middle Eastern, South Asian, and North African cultures (Hepp et al., 2012). Historical contamination of children's toys with antimony-containing compounds presents additional exposure risks, particularly for vulnerable pediatric populations (Greenway & Gerstenberger, 2010). The convergence of these multiple exposure pathways—dietary, dermal, and environmental—necessitates a comprehensive understanding of antimony toxicology and evidence-based detoxification strategies.

This article examines the scientific literature on antimony exposure sources, absorption mechanisms, toxicological effects, and research-supported approaches to reducing body burden and mitigating health impacts. Understanding antimony's behavior in biological systems and implementing appropriate prevention and detoxification measures represents an essential yet underappreciated component of contemporary environmental health practice.

Antimony Exposure from PET Plastic Bottles: A Global Health Concern

Polyethylene terephthalate (PET) has become the dominant material for beverage containers worldwide, with global production exceeding 30 million tons annually. The polymerization process used to manufacture PET requires antimony trioxide as a catalyst, with residual antimony remaining in the finished product at concentrations typically ranging from 200 to 300 mg/kg (Westerhoff et al., 2008). Under certain conditions, this antimony can migrate from the plastic matrix into beverages, creating a potential chronic exposure pathway affecting billions of consumers globally.

Leaching Mechanisms and Influencing Factors

Research has consistently demonstrated that antimony leaches from PET bottles into contained beverages, with migration rates influenced by multiple factors including temperature, storage duration, pH, and beverage composition. Shotyk and Krachler (2007) conducted seminal research documenting antimony concentrations in bottled water significantly exceeding levels found in natural groundwater, with concentrations increasing substantially during storage. Their findings revealed that antimony levels in mineral water stored in PET bottles for three months increased by factors of up to 90% compared to initial measurements, demonstrating that leaching is an ongoing process rather than merely an immediate manufacturing residue issue.

Temperature represents the most critical variable governing antimony migration from PET. Studies have shown that elevated temperatures dramatically accelerate leaching rates, with antimony concentrations increasing exponentially as temperatures rise above 25°C (Keresztes et al., 2009). This temperature dependence has profound implications for beverage safety in regions with hot climates or where bottles are stored in warm conditions such as vehicles, warehouses, or retail displays exposed to sunlight. Research by Keresztes and colleagues (2009) demonstrated that water stored at 60°C for 10 days contained antimony levels exceeding 100 µg/L—well above the World Health Organization guideline of 20 µg/L for drinking water.

The pH of beverages also influences antimony leaching, with acidic drinks promoting greater migration. Carbonated beverages, fruit juices, and flavored waters with pH below 4 show enhanced antimony leaching compared to neutral pH water (Westerhoff et al., 2008). This pH effect is particularly concerning given that many popular bottled beverages are acidic, potentially exposing consumers to elevated antimony levels even under ambient storage conditions. Additionally, repeated heating cycles, such as those occurring during transport and storage, create cumulative effects that progressively increase antimony content in beverages (Keresztes et al., 2009).

Toxicological Implications and Health Concerns

Antimony's toxicological profile shares similarities with arsenic, its chemical analog in the periodic table. Antimony exposure has been associated with respiratory irritation, cardiovascular effects, and potential carcinogenicity, though human epidemiological data remains limited compared to more extensively studied heavy metals (Sundar & Chakravarty, 2010). The International Agency for Research on Cancer (IARC) classifies antimony trioxide as a possible human carcinogen (Group 2B), based primarily on animal studies demonstrating lung tumor formation following inhalation exposure.

Chronic low-level antimony exposure from bottled beverages represents a distinct toxicological scenario from acute occupational or environmental exposures. While individual consumption episodes involve antimony levels typically below acute toxicity thresholds, the cumulative burden from daily consumption over years or decades raises concerns about chronic health effects. Carneado and colleagues (2015) noted that antimony possesses both redox-active properties and the ability to bind to sulfhydryl groups in proteins, potentially disrupting enzymatic functions and generating oxidative stress—mechanisms implicated in numerous chronic diseases.

The antimony species present in beverages predominantly exists as antimony(III), the more toxic form compared to antimony(V). This speciation is critical because antimony(III) demonstrates greater cellular uptake and biological activity (Filella et al., 2002). Furthermore, antimony's chemical similarity to arsenic suggests it may interfere with similar metabolic pathways, though antimony metabolism and elimination mechanisms remain incompletely characterized in humans. Research indicates that antimony undergoes limited methylation in mammals, contrasting with arsenic metabolism, and is primarily excreted via urine with a biological half-life ranging from several days to weeks depending on exposure route and speciation (Sundar & Chakravarty, 2010).

Regulatory Landscape and Public Health Response

Despite mounting evidence of antimony leaching from PET bottles, regulatory responses have been inconsistent globally. The World Health Organization established a guideline value of 20 µg/L for antimony in drinking water, while the European Union and United States EPA have set limits of 5 µg/L and 6 µg/L respectively (Shotyk & Krachler, 2007). However, these standards apply specifically to tap water and may not adequately address the distinct exposure scenario presented by bottled beverages, particularly under conditions promoting enhanced leaching.

Several studies have documented antimony levels in commercially available bottled waters exceeding regulatory limits, especially in products stored under suboptimal conditions. Westerhoff and colleagues (2008) analyzed 15 brands of bottled water in the United States and found that while most samples contained antimony below 1 µg/L when fresh, extended storage at elevated temperatures resulted in exceedances of drinking water standards in multiple samples. This variability in antimony content—dependent on storage conditions outside regulatory control—creates a challenge for establishing consistent consumer protection.

Public health recommendations increasingly emphasize minimizing PET bottle exposure to heat and sunlight, limiting storage duration, and preferentially choosing alternative packaging materials such as glass or stainless steel for long-term beverage storage. Some manufacturers have explored antimony-free PET production using alternative catalysts such as titanium or germanium compounds, though these technologies have not achieved widespread commercial adoption due to cost considerations and technical challenges (Welle & Franz, 2011).

Traditional Cosmetics Containing Antimony: Ancient Practices and Modern Risks

The use of antimony-containing compounds in cosmetics represents one of humanity's oldest continuous exposure pathways, with archaeological evidence documenting kohl application dating back to ancient Egypt over 4,000 years ago. These traditional eye cosmetics, known variously as kohl, surma, kajal, or al-kahal depending on cultural context, remain widely used across Middle Eastern, South Asian, North African, and some Mediterranean communities for both cosmetic and purported medicinal purposes (Hepp et al., 2012).

Traditional kohl formulations typically contain antimony sulfide (Sb₂S₃, stibnite) as a primary ingredient, often combined with other materials including galena (lead sulfide), various plant materials, camphor, and other substances depending on regional traditions and intended applications. The characteristic dark gray or black color derives from these metal sulfides, which have been valued not only for aesthetic appeal but also for traditional beliefs regarding eye health protection and spiritual benefits (Al-Ashban et al., 2004).

The preparation of traditional kohl often involves artisanal processing methods passed through generations, with ingredients sourced from mineral deposits and processed using techniques that may introduce additional contaminants. Modern commercial versions marketed in cosmetic stores may contain antimony compounds synthesized through industrial processes or may use alternative ingredients attempting to replicate traditional formulations while theoretically reducing heavy metal content. However, studies consistently demonstrate that many commercial kohl products contain substantial antimony, lead, and other toxic metals regardless of marketing claims (Hepp et al., 2012).

Exposure Pathways and Absorption

The application of kohl to the eyes creates multiple exposure pathways with distinct absorption characteristics. Direct ocular exposure occurs through contact with conjunctival membranes, which are highly vascularized and capable of absorbing antimony compounds. Nasolacrimal drainage transports kohl particles into the nasal passages and potentially to the gastrointestinal tract via mucociliary clearance and swallowing. Additionally, hand-to-mouth behavior, particularly in children whose caregivers apply kohl, creates an oral ingestion pathway (Al-Hazzani & Krahn, 2012).

Research examining blood antimony levels in kohl users demonstrates significantly elevated concentrations compared to non-users. Al-Ashban and colleagues (2004) measured blood antimony concentrations in regular kohl users in Saudi Arabia and found levels several-fold higher than background levels in control populations. These findings confirm that antimony from kohl applications undergoes systemic absorption, creating body burden accumulation with repeated use. Particularly concerning are practices involving kohl application to infants and young children, where developing organ systems may exhibit enhanced vulnerability to antimony's toxic effects (Al-Hazzani & Krahn, 2012).

Health Effects and Clinical Concerns

Clinical literature documents numerous adverse effects associated with antimony-containing kohl use, ranging from local irritation to systemic toxicity. Ocular effects include conjunctivitis, keratitis, and chronic inflammation of periocular tissues. Case reports have documented lead and antimony poisoning in children whose caregivers regularly applied kohl, presenting with symptoms including developmental delays, anemia, gastrointestinal disturbances, and neurological abnormalities (Al-Hazzani & Krahn, 2012).

The synergistic toxicity of antimony combined with lead—both commonly present in traditional kohl—may produce additive or potentiated adverse effects. Lead's well-documented neurotoxicity, particularly in children, compounds the oxidative stress and cellular damage associated with antimony exposure. Hepp and colleagues (2012) analyzed commercial kohl products available in German markets and found that 8 of 10 tested products contained lead concentrations exceeding regulatory limits, with several products also containing elevated antimony levels. These findings demonstrate that kohl-associated heavy metal exposure remains a contemporary public health concern even in regulated markets.

 Regulatory Challenges and Cultural Considerations

Addressing antimony exposure from traditional cosmetics presents unique challenges due to cultural significance, informal distribution networks, and varying regulatory frameworks across jurisdictions. In the United States, the Food and Drug Administration prohibits kohl products due to heavy metal content, yet they remain readily available through ethnic markets, online retailers, and international travel. European regulations similarly restrict heavy metal content in cosmetics, though enforcement faces practical limitations with imported and artisanal products (Hepp et al., 2012).

Public health interventions must balance respect for cultural practices with clear communication about health risks, particularly regarding vulnerable populations. Educational campaigns emphasizing risks to children have achieved some success in reducing pediatric kohl application, though adult use remains prevalent in many communities. The development and promotion of antimony-free and lead-free alternatives that preserve aesthetic and cultural characteristics represents a promising harm reduction approach, though consumer acceptance requires careful navigation of traditional beliefs and preferences (Al-Hazzani & Krahn, 2012).

 Antimony Contamination in Vintage Toys: Historical Perspective and Persistent Risks

Children's toys represent an often-overlooked source of heavy metal exposure, with antimony contamination occurring through multiple mechanisms including use as a pigment, flame retardant, and polymerization catalyst in plastics. While contemporary regulations have reduced antimony content in newly manufactured toys in many jurisdictions, vintage toys—particularly those manufactured before the 1970s—may contain substantial antimony levels posing risks through direct contact, mouthing behavior, and deterioration releasing antimony-containing dust (Greenway & Gerstenberger, 2010).

Historical Use and Contamination Sources

Antimony compounds found diverse applications in toy manufacturing throughout the 20th century. Antimony trioxide served as an opacifying agent in white and colored enamels applied to metal toys, as a flame retardant synergist in plastic formulations, and as a catalyst in polyester and synthetic fiber production used in stuffed toys and dolls (Weidenhamer et al., 2017). The pigment known as Naples Yellow, containing lead antimonate, appeared in painted wooden toys and ceramic glazes. Additionally, antimony alloys were used in die-cast metal toys due to their low melting point and excellent casting properties.

The widespread use of antimony in toy manufacturing occurred during an era of minimal regulatory oversight regarding heavy metal content in consumer products. Concentrations of antimony in vintage toys can reach several thousand parts per million, particularly in painted surfaces and plastic components (Greenway & Gerstenberger, 2010). As these materials age and degrade, antimony becomes increasingly bioavailable through paint chip formation, plastic deterioration, and surface dust generation—all of which can be ingested or inhaled by children playing with these items.

Exposure Assessment and Risk Characterization

Quantifying antimony exposure from vintage toys requires consideration of multiple factors including toy condition, frequency of use, child behavior patterns, and antimony bioavailability. Greenway and Gerstenberger (2010) conducted comprehensive analysis of antique and collectible toys, finding that approximately 10% of tested items contained antimony at levels exceeding 60 µg/cm² in surface wipes—a level indicating potential health concern. Their research employed bioaccessibility testing using simulated gastric fluid to estimate the fraction of antimony that would be absorbed if toy materials were ingested, finding substantial variability depending on antimony speciation and matrix composition.

Children face particular vulnerability to toy-associated antimony exposure due to hand-to-mouth behavior, longer biological residence times for absorbed metals, and developing organ systems more susceptible to toxic insult. The U.S. Consumer Product Safety Commission has established limits for antimony in children's products of 60 ppm in accessible materials, though this standard applies only to new products and does not address legacy items in homes, daycare centers, or secondhand markets (Weidenhamer et al., 2017).

Surface coating deterioration represents a critical factor in exposure risk from vintage toys. Painted surfaces may develop fine cracks, chips, or chalking that creates ingestible particles with enhanced bioavailability compared to intact coatings. Weidenhamer and colleagues (2017) demonstrated that aged painted toys shed particles containing not only antimony but also lead, cadmium, and chromium, creating complex mixture exposures that may exhibit additive or synergistic toxicity. Their findings underscore that vintage toys should not be considered safe for children's play merely based on visual inspection.

Risk Management and Consumer Protection

Managing antimony exposure from vintage toys requires multi-faceted approaches including consumer education, screening protocols, and appropriate use decisions. Parents, collectors, and childcare providers should be aware that toys manufactured before 1980—particularly those with painted surfaces, die-cast metal components, or plastic parts—may contain hazardous levels of antimony and other heavy metals. Professional testing using X-ray fluorescence (XRF) analyzers can provide rapid screening for elevated antimony, though specialized laboratory analysis may be necessary for definitive quantification and speciation (Greenway & Gerstenberger, 2010).

Appropriate use decisions should consider toy condition, child age, and play patterns. Well-preserved vintage toys may be appropriate for display or supervised adult collecting while remaining unsuitable for children's active play. When antimony contamination is confirmed or suspected, removal from children's access and proper disposal according to hazardous waste guidelines prevents ongoing exposure. The romanticized appeal of vintage toys must be balanced against documented health risks, particularly for items showing signs of deterioration or damage (Weidenhamer et al., 2017).

General Heavy Metal Detoxification: Principles, Evidence, and Critical Caveats

The concept of "detoxification" from heavy metals including antimony has generated substantial popular interest, spawning a commercial industry promoting various products and protocols claiming to reduce body burden and improve health outcomes. However, scientific evaluation of heavy metal detoxification requires careful distinction between evidence-based medical chelation therapy for acute poisoning, supportive nutritional approaches that may enhance endogenous detoxification mechanisms, and unsubstantiated commercial products lacking rigorous clinical validation.

Medical Chelation Therapy

Chelation therapy using pharmaceutical agents represents the evidence-based intervention for significant heavy metal poisoning, with well-established protocols for lead, mercury, arsenic, and iron toxicity. Chelating agents—molecules with multiple binding sites that form stable complexes with metal ions—increase urinary or fecal metal excretion, reducing body burden and mitigating toxicity (Flora & Pachauri, 2010). Common chelating agents include dimercaptosuccinic acid (DMSA), dimercaptopropanol (British Anti-Lewisite or BAL), calcium disodium EDTA, and d-penicillamine, each with distinct pharmacokinetic properties, metal affinities, and adverse effect profiles.

For antimony specifically, chelation therapy protocols have been adapted from arsenic poisoning treatment, given chemical similarities between these metalloids. DMSA has shown efficacy in enhancing antimony elimination in animal models and limited human case reports, though systematic clinical trials are lacking (Sundar & Chakravarty, 2010). BAL, historically used for arsenic and antimony toxicity, has largely been supplanted by DMSA due to superior tolerability and efficacy. However, it is critical to emphasize that pharmaceutical chelation therapy is appropriate only for documented significant poisoning and must be administered under medical supervision due to potential adverse effects including mineral depletion, redistribution of metals to sensitive tissues, and allergic reactions (Flora & Pachauri, 2010).

Endogenous Detoxification Systems and Nutritional Support

Beyond pharmaceutical chelation for acute poisoning, the human body possesses endogenous mechanisms for processing and eliminating toxic metals including antimony. These systems involve conjugation reactions, binding to metallothioneins and other metal-binding proteins, biliary excretion, and renal elimination. Nutritional approaches to supporting these endogenous pathways represent a distinct and potentially valuable intervention, though claims must be evaluated critically and distinguished from unsupported "detox" marketing (Sears, 2013).

Glutathione, the body's primary intracellular antioxidant and phase II detoxification molecule, plays a crucial role in heavy metal metabolism through conjugation reactions that facilitate excretion. Maintaining adequate glutathione levels through diet or supplementation with precursors such as N-acetylcysteine (NAC) may support metal elimination, though clinical evidence specifically for antimony remains limited. NAC supplementation has demonstrated efficacy in arsenic poisoning, increasing urinary arsenic excretion and reducing oxidative stress markers, suggesting potential benefit for the chemically related antimony (Flora & Pachauri, 2010).

Selenium presents particular interest for antimony detoxification given its ability to form complexes with various metals and metalloids. Research has shown that selenium supplementation can reduce arsenic toxicity and enhance excretion, potentially through formation of seleno-bis(S-glutathionyl) arsinium ion complexes (Zwolak & Zaporowska, 2012). Given antimony's chemical relationship to arsenic, similar selenium-antimony interactions may occur, though direct clinical evidence is lacking. Selenium supplementation must be approached cautiously given the narrow therapeutic window between beneficial and toxic doses, with recommended intakes not exceeding 400 µg daily for adults.

Dietary Approaches and Phytochemicals

Certain dietary components have demonstrated ability to influence heavy metal absorption, distribution, or elimination through various mechanisms. Fiber, particularly soluble fiber and certain complex polysaccharides, can bind metals in the gastrointestinal tract, reducing absorption and enhancing fecal excretion. Modified citrus pectin has shown promise in animal studies for increasing urinary excretion of lead, cadmium, and mercury without depleting essential minerals, though human clinical data remains limited (Eliaz et al., 2006).

Cruciferous vegetables containing sulforaphane and other isothiocyanates upregulate phase II detoxification enzymes including glutathione S-transferases, potentially enhancing conjugation and elimination of toxic compounds including heavy metals. Cilantro (coriander leaves) has gained popularity in alternative health communities as a "natural chelator," though scientific evidence supporting this claim remains controversial. While some animal studies suggest cilantro extracts may enhance lead excretion, well-controlled human clinical trials are lacking, and mechanisms remain unclear (Aga et al., 2001).

Chlorella, a freshwater green alga, has been promoted for heavy metal detoxification based on its high chlorophyll content and cell wall polysaccharides that may bind metals. Animal research suggests chlorella supplementation can reduce tissue accumulation of cadmium and methylmercury, potentially through both reduced intestinal absorption and enhanced fecal elimination (Uchikawa et al., 2011). However, human clinical evidence remains limited, and chlorella products vary substantially in composition and quality. Critical evaluation is necessary given that chlorella may also accumulate toxic metals from contaminated growth environments, potentially increasing rather than decreasing exposure.

Safety Considerations

Several critical caveats warrant emphasis when discussing heavy metal detoxification. First, the majority of "detox" products marketed to consumers lack rigorous clinical evidence supporting efficacy claims. Systematic reviews of chelation and detoxification interventions consistently note the paucity of high-quality human trials, with most evidence derived from animal models or mechanistic studies that may not translate to clinically meaningful human benefits (Ernst, 2012).

Second, aggressive or inappropriate chelation can cause harm through several mechanisms. Chelating agents mobilize metals from storage tissues, potentially redistributing them to more vulnerable organs such as the brain before elimination occurs. This redistribution effect has been documented with DMSA and other agents, necessitating careful dosing protocols and contraindications for certain patient populations (Flora & Pachauri, 2010). Additionally, chelating agents may deplete essential minerals including zinc, copper, and iron, requiring monitoring and potential supplementation during treatment.

Third, the concept of "detoxification" should not distract from the primary preventive principle: reducing ongoing exposure. For antimony specifically, this means minimizing consumption of beverages stored in PET bottles under suboptimal conditions, avoiding antimony-containing cosmetics, and preventing children's access to contaminated vintage toys. No detoxification protocol can fully compensate for continued high-level exposure, making source reduction the fundamental intervention (Sears, 2013).

Finally, individuals concerned about antimony exposure should pursue proper medical evaluation including measurement of blood or urinary antimony levels before initiating any detoxification protocol. Symptoms attributed to "heavy metal toxicity" frequently have other causes requiring different treatments, and inappropriate chelation therapy in the absence of documented poisoning exposes patients to unnecessary risks without benefit. Consultation with physicians experienced in occupational and environmental medicine or medical toxicology is essential for appropriate evaluation and management (Ernst, 2012).

Evidence-Based Strategies for Reducing Antimony Burden

Synthesizing current scientific understanding, several evidence-based strategies emerge for reducing antimony exposure and supporting elimination:

Exposure Prevention (Primary Strategy):
- Minimize consumption of beverages stored in PET bottles, particularly those exposed to heat or stored for extended periods
- Choose alternative packaging materials (glass, stainless steel) when possible
- Avoid traditional kohl cosmetics containing antimony or lead; use certified antimony-free alternatives
- Screen vintage toys for heavy metal contamination before allowing children's access
- Be aware of occupational and environmental exposure sources in specific industries

Nutritional Support for Endogenous Detoxification:
- Ensure adequate dietary protein intake to support glutathione synthesis
- Consider N-acetylcysteine supplementation (600-1200 mg daily) under medical supervision for supporting glutathione status
- Maintain adequate selenium intake through diet (Brazil nuts, seafood, whole grains) or supplementation (100-200 µg daily) within safe limits
- Increase dietary fiber from whole plant foods to enhance intestinal metal binding and elimination
- Consume cruciferous vegetables regularly to support phase II detoxification enzyme activity

Medical Intervention When Indicated:
- Seek proper medical evaluation if significant antimony exposure is suspected
- Pursue blood or urinary antimony measurement to quantify body burden
- Consider pharmaceutical chelation therapy only under medical supervision for documented significant poisoning
- Monitor for potential adverse effects and mineral depletion during any chelation protocol

General Health Optimization:
- Maintain adequate hydration to support renal elimination pathways
- Ensure sufficient intake of calcium, iron, and zinc, as deficiencies can enhance absorption of toxic metals
- Engage in regular physical activity, which may enhance various elimination pathways
- Minimize alcohol consumption and other hepatotoxins that impair liver detoxification capacity

Conclusion

Antimony represents an underrecognized environmental health concern with multiple exposure pathways affecting diverse populations globally. The leaching of antimony from PET plastic bottles into beverages, particularly under conditions of elevated temperature and extended storage, creates a ubiquitous chronic exposure affecting billions of consumers. Traditional cosmetics containing antimony compounds continue to expose users—including vulnerable infants and children—to significant quantities of this toxic metalloid. Historical contamination of vintage toys with antimony and other heavy metals persists as a potential exposure source when these items remain accessible to children.

Understanding antimony toxicology and implementing appropriate prevention and detoxification strategies requires integrating insights from environmental science, toxicology, nutrition, and clinical medicine. While pharmaceutical chelation therapy represents the evidence-based intervention for significant poisoning, most individuals face the challenge of chronic low-level exposure requiring a focus on source reduction and support for endogenous detoxification mechanisms. Nutritional approaches including adequate glutathione precursors, selenium within safe limits, increased dietary fiber, and consumption of cruciferous vegetables may support metal elimination, though clinical evidence specific to antimony remains limited.

Critical evaluation of detoxification claims is essential given the proliferation of commercial products and protocols lacking rigorous scientific validation. The fundamental principle remains clear: preventing exposure through informed consumer choices and regulatory protections represents the most effective strategy for minimizing antimony-associated health risks. As research continues to elucidate antimony's environmental distribution, human exposure patterns, and toxicological mechanisms, public health interventions can become increasingly targeted and effective.

Future research priorities should include: (1) comprehensive assessment of antimony exposure through multiple pathways and cumulative burden quantification; (2) epidemiological studies examining health outcomes associated with chronic low-level antimony exposure; (3) controlled clinical trials evaluating nutritional and pharmaceutical interventions for enhancing antimony elimination; (4) development and implementation of antimony-free alternatives for PET production and traditional cosmetics; and (5) improved regulatory frameworks addressing antimony in consumer products across jurisdictions. Addressing these knowledge gaps will enable more effective protection of public health from this widespread yet underappreciated environmental contaminant.

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