Oxidative Stress in Mining Workers: Dietary Antioxidants, Nutritional Interventions, and Workplace Nutrition Strategies

Introduction

Mining remains a critical part of today’s economies, but the work poses complex workplace hazards that can disrupt cellular redox homeostasis.^1,2 Respirable coal and mineral dusts, crystalline silica, metal-rich dusts, PAHs, diesel emissions, heat, hypoxia, and a challenging physical workload are all potential exposures for miners depending on the commodity, extraction method, and work environment. These exposures seldom happen on their own. Their biological effects can be influenced by their size, surface reactivity, mineralogical and chemical composition and the intensity of their exposure. Also, the timing of their shift, smoking, nutritional status, and other coexisting diseases play a role.^1,3 For example, quartz, siderite, anatase, and redox-active trace elements associated with its oxidative potential may be present in underground coal-mine dust.⁴

Excessive amounts of ROS and RNS cause oxidative stress when they overwhelm the body’s intrinsic antioxidant defenses. Oxidants may be generated by metal redox cycling, reactive particle surfaces, or indirectly by oxidase activity, mitochondrial leakage, and/or persistent activation of inflammatory cells in the mining environment.^5,6,7 The resulting imbalance can alter the activities of glutathione peroxidase, catalase, and superoxide dismutase, as well as glutathione status.¹ Examples of oxidative injury include lipid peroxidation, protein oxidation, DNA damage, mitochondrial depolarization, lysosomal destabilization, and inflammatory signaling.^8,9 They are not independent processes; rather, they are interconnected and can lead to pulmonary and systemic cellular dysfunction.⁹ 

Studies of workers show redox disruptions across several mining industries. SOD, CAT, and GSH are altered in coal miners, particularly those working underground for longer hours and with high exposure.¹ In chromite miners, urinary chromium, lead, cadmium, and nickel have been associated with increased MDA or altered SOD.¹⁰ The lymphocytes of lead-zinc miners were found to be less viable. They had lower levels of reduced glutathione, higher levels of oxidized glutathione, and higher levels of ROS, mitochondrial depolarization, and lysosomal damage.⁸ Additionally, oxidative imbalance, diminished antioxidant defenses, inflammatory alterations, and compromised pulmonary function were observed in miners exposed to silica.¹¹ A significant amount of this information is cross-sectional; however, there is no evidence that any specific oxidative biomarker reliably predicts future disease.¹² 

Vitamins, minerals, amino acids, and plant-derived bioactive compounds support endogenous antioxidant systems, making nutrition important to redox homeostasis. Vitamins C and E work in complementary aqueous and lipid environments, while selenium, zinc, copper, and manganese support antioxidant-enzyme systems.^13,14 Mechanistic plausibility does not prove clinical efficacy. The main occupational supplementation study examined biomarkers rather than clinical outcomes in small, non-randomized groups, and the mining literature has more observational evidence on oxidative imbalance than controlled evidence on diet or nutritional interventions.¹⁵ Due to this gap, exposure-related oxidative stress must be distinguished from nutritional strategies that improve clinical outcomes. Nutrition should support worker health, not replace dust suppression, ventilation, exposure monitoring, respiratory protection, or other occupational controls.¹⁶ 

This narrative review aims to (1) synthesize mining-specific evidence on occupational exposures, mechanisms, biomarkers, and health outcomes related to oxidative stress; (2) evaluate dietary factors, antioxidant nutrients, supplements, functional foods, and workplace nutrition while explicitly distinguishing observational from intervention evidence; (3) assess methodological limitations and safety considerations; and (4) identify priorities. Heat stress, hypoxia, and other occupational co-exposures are only included if they affect oxidative burden, hydration, nutrition, or workplace nutrition strategy design and interpretation.

Materials and Methods 

This narrative review was chosen due to its coverage of diverse evidence, encompassing mining epidemiology, mechanistic studies, biomarker research, nutrition, supplementation, and workplace health interventions, which lack the uniformity required for quantitative pooling. PubMed/MEDLINE, Scopus, Web of Science, and Google Scholar were searched without a lower publication-date limit through July 31, 2026. Search concepts included combinations of “miner*,” “mining worker*,” “coal,” “silica,” “metal*,” “polycyclic aromatic hydrocarbons,” “oxidative stress,” “reactive oxygen species,” “antioxidant*,” “diet,” “nutrition,” “micronutrient*,” “functional food*,” and “supplement*.” Studies involving mining workers were given priority in human research. Eligible evidence focused on mining exposures, oxidative or inflammatory biomarkers, antioxidant status, health outcomes, dietary factors, supplements, functional foods, and workplace nutrition. In the absence of mining-specific evidence, studies from non-mining occupations, experimental mechanistic research, systematic reviews, and authoritative guidance were utilized to elucidate mechanisms, safety, or workplace practices. Publications were excluded if they failed to address the review questions or if the source and reported findings could not be verified. Records that may be relevant were evaluated based on their titles and abstracts, followed by a thorough assessment of the full texts. Additionally, reference lists and focused supplementary searches were employed to uncover further pertinent studies. We synthesized evidence in a narrative format and categorized it as observational human studies, experimental or mechanistic research, nutritional interventions, or higher-level guidelines. Interpretation considered study design, population, sample size, exposure assessment, direct relevance to mining workers, consistency of findings, and whether outcomes were biomarkers or clinical endpoints. No meta-analysis or formal risk-of-bias tool was utilized. Consequently, publication bias, selection bias, residual confounding, and subjective interpretation remain limitations of this narrative approach. Numerical findings were presented solely when directly accessible from the referenced study; no statistical re-analysis was conducted.

Results

 Sources Of Oxidative Stress In Mining Work

Mining workers are usually exposed to multiple oxidant-generating hazards.¹⁷ Respirable particles, crystalline silica, transition metals, and other redox-active components are found in coal and mineral dusts; the oxidative potential of these constituents is dependent on their size, surface area, mineralogy, and chemical makeup. Quartz, siderite, anatase, and other potentially hazardous substances that can contribute to the generation of ROS have been found in dust collected from underground coal mines.^4,17 In addition, disruption of glutathione and antioxidant enzymes has been observed among coal miners, and this disruption is more severe among underground workers and those with longer exposure.^1,4 Metal mining introduces additional oxidative risks. Chromium, lead, cadmium, nickel, mercury, iron, and manganese may contribute to redox cycling, disruption of mitochondrial function, and/or reduced endogenous antioxidant defenses. The urinary metal levels were higher among chromite miners and were associated with increased lipid peroxidation among extraction miners.¹⁰ PAHs generated by incomplete combustion, diesel-powered machinery, blasting, and coal-related processes can also contribute to oxidative stress.¹⁸ Some of these interactions have not been well documented, but are known to be more pronounced in the presence of heat, hypoxia, physical exertion, smoking, and poor nutrition; however, there is limited direct mining-specific evidence for some of these interactions (Table 1).¹⁰

Table 1: Principal occupational exposures associated with oxidative stress in mining work

Mechanisms Of Mining-Related Oxidative Damage

Silica and respirable coal particles lodge in the distal airways, where they interact with alveolar epithelial cells and macrophages. In studies of coal miners’ bronchoalveolar health, respirable coal dust and quartz burden have been linked to elevated levels of alveolar macrophages, neutrophils, reactive oxygen species, and inflammatory responses.^21,22 Particle-surface radicals, redox-active metals, and macrophage responses can contribute to oxidant generation, as shown in experimental studies involving silica.^23,24 When oxidant production exceeds antioxidant capacity, glutathione and antioxidant enzymes may change, leading to a transition toward oxidative stress.^1,5 Silica phagocytosis can promote lysosomal destabilization, activate the NLRP3 inflammasome, and lead to cytokine release from macrophages.^9,25 A small comparative study of 10 lead-zinc miners and 10 controls indicated systemic cellular effects: miners’ lymphocytes showed elevated GSSG and ROS, reduced GSH and viability, reduced mitochondrial membrane potential, and signs of lysosomal damage.⁸ Lipid peroxidation, the formation of 8-isoprostane, protein carbonyls, and DNA damage have been documented in studies involving mining workers.^5,15,26,27 Together, these findings indicate an interaction among oxidative, mitochondrial, lysosomal, inflammatory, and genomic pathways, although several mechanistic links remain not fully established in long-term human mining studies. (Fig. 1).

Figure 1: Mechanism of mining-related oxidative injury Click here to view Figure

Biomarkers Of Oxidative Stress Among Mining Workers

While biomarkers of lipid oxidation, antioxidant defense, DNA damage, protein oxidation, and total redox capacity have been employed in mining studies, none of these markers provides a comprehensive assessment of systemic oxidative stress.¹² Thiobarbituric acid assays are not chemically specific, but MDA and thiobarbituric acid-reactive substances are often used as markers of lipid peroxidation. Coal, chromite, zinc-lead, and artisanal gem miners have been found to have higher TBARS, MDA, or related lipoperoxidation measures.^5,10,28,29 By-products of lipid peroxidation by free radicals are more chemically specific, such as the F₂-isoprostanes.³⁰ Cumulative exposure over successive shifts may be more readily detected than exposure during a single shift, with exhaled breath condensate 8-isoprostane levels higher among coal miners than in the control group after 3 consecutive working days.²⁶ Another study from the same mine reported a positive association between plasma 8-isoprostane and blood lead.³¹ The activity of antioxidants may be used to interpret increases or decreases, which may be due to adaptation, inhibition, depletion, disease stage, or confounding factors. Age affected differences in plasma GPx and TAC, but no differences were observed in erythrocyte enzymes or total plasma antioxidants between retired miners with and without pneumoconiosis.³² Erythrocyte Cu/Zn-SOD was higher in underground miners than in surface miners among active coal miners. Thus, a panel of exposure biomarkers, oxidative damage products, antioxidant defenses, inflammation, and clinical measures is preferable to a single marker ¹² (Table 2).

Table 2: Biomarkers used to assess oxidative stress and related exposure among mining workers

Health Consequences Of Oxidative Stress In Mining Workers

The lungs serve as the main targets for inhaled mine dust. In mine workers exposed to silica, reports show lower FEV₁, FVC, FEV₁/FVC, PEF, and MEF, along with increased lipid peroxidation and oxidative-stress indices. Additionally, catalase, SOD, GPx, and TAC were reduced, along with evidence of systemic inflammation.¹¹ These cross-sectional findings indicate a relationship between redox imbalance and pulmonary dysfunction, yet they do not confirm oxidative stress as the only causal mechanism. Ongoing oxidative and inflammatory reactions to crystalline silica may also contribute to the development and progression of silicosis.³⁴ Genotoxic effects have been observed in various mining populations. Artisanal gold miners exposed to mercury showed changes in LINE1 and Alu(Yb8) methylation, along with elevated peripheral-blood 8-OHdG levels. In contrast, coal miners showed reduced GSH levels, increased MDA, and more significant DNA damage by comet assay compared with controls.²⁷ Exposure to coal dust has been linked to increased postprandial glucose levels, changes in antioxidant-enzyme activity, and lipid peroxidation.³⁵ Exposure to PAH among coal miners has been linked to changes in neurotransmitters and neurobehavioral patterns, although a definitive connection to oxidative stress as the mediating pathway has yet to be established.^18,36 Overall, most evidence is observational and cross-sectional; therefore, oxidative biomarkers should be viewed as indicators of exposure or biological response rather than confirmed predictors of future disease (Fig. 2).

Figure 2: Potential health outcomes associated with mining-related oxidative and inflammatory imbalance Click here to view Figure

Dietary Antioxidants Relevant To Mining-Related Oxidative Stress

Dietary antioxidants and nutrients related to antioxidants bolster the body’s natural redox defense via unique mechanisms. Vitamin E is a lipid-soluble antioxidant that interrupts the chain reaction of membrane lipid peroxidation, while vitamin C primarily functions in aqueous environments and has the ability to regenerate oxidized α-tocopherol.^37,38,39 Certain carotenoids have the ability to quench reactive species, whereas polyphenols may influence redox-sensitive and inflammatory signaling. The biological effects of these compounds depend on their chemical structure, the food matrix, metabolism, dosage, and baseline nutritional status. Manganese serves as a cofactor for mitochondrial Mn-SOD, while copper and zinc are integral components of Cu/Zn-SOD. Selenium is also incorporated into glutathione peroxidases and various other selenoproteins.^40,41 These nutrients are essential for physiological functions; however, an excessive intake can be detrimental, especially for individuals exposed to metals in their work environment. Evidence for direct miner-specific nutritional interventions is currently quite limited (Table 3).

Table 3: Dietary antioxidants and antioxidant-related nutrients potentially relevant to mining workers

Nutritional Supplementation And Functional-Food Interventions

Intervention evidence is much more limited than observational evidence of oxidative imbalance among miners. The principal human occupational intervention involved administering vitamin E (800 mg/day) and vitamin C (500 mg/day) for a duration of 6 months to six small groups that were exposed, either directly or indirectly, to airborne contamination from coal mining or medical-waste incineration. TBARS and protein carbonyls decreased, whereas glutathione, α-tocopherol, and certain antioxidant-enzyme measures increased or were restored.¹⁵ These findings indicate a change in biomarkers, rather than the prevention or treatment of diseases related to mining. Interpretation is limited by the pre-post design, the lack of reported randomization or placebo control, the heterogeneous exposure groups, the small sample size of 20 participants per group, the high supplemental doses, and the absence of clinical outcomes.

The literature reviewed, and the targeted supplementary searches, did not reveal strong controlled trials specific to miners regarding antioxidant beverages, polyphenol concentrates, selenium-enriched foods, probiotics, or other specially formulated functional foods. Consequently, their effectiveness in addressing oxidative stress related to mining has yet to be established. Enhancement in an oxidative biomarker should not be viewed as proof that an intervention averts pneumoconiosis, cardiovascular disease, cancer, or occupational injury. Wider randomized evidence does not support the assumption that clinical benefits arise from antioxidant supplementation based solely on biochemical antioxidant activity.⁴² Targeted supplementation is best justified when dietary assessment, biochemical testing, or clinical evaluation reveals inadequate intake, deficiency, malabsorption, or another acknowledged indication. Future trials should clearly define the nutrient form, dose, duration, product quality, baseline nutritional status, adherence, medication use, adverse events, and clinically meaningful outcomes, while adhering to best-practice engineering and occupational controls (Table 4).

Table 4: Potential nutritional supplementation and functional-food interventions for mining workers

Workplace Nutrition Strategies For Mining Workers

Workplace nutrition should be part of the broader occupational health system rather than a replacement for it. Nutrition cannot stop the inhalation or systemic absorption of silica, coal dust, or toxic metals.⁴³ Elimination, substitution, and engineering controls are the most favored methods for managing hazardous exposure, succeeded by administrative controls and suitable PPE. A practical nutrition program may evaluate dietary intake, food access or insecurity, anthropometry, cardiometabolic risk, smoking, alcohol consumption, medication usage, and clinically significant micronutrient deficiencies. General guidance for a healthy diet emphasizes the importance of increasing the intake of vegetables, fruits, whole grains, legumes, nuts, and suitable protein sources, while also advising the reduction of highly processed and fried foods, processed meats, excessive sodium, and sugary drinks.⁴⁴ Providing meals sensitive to timing may reduce dependence on energy-dense snacks and improve access to well-balanced meals. Cool drinking water should be easily accessible near hot work areas; electrolyte-containing fluids may be suitable during extended periods of sweating but are not necessary for every worker or shift.⁴⁵ Program evaluation may encompass aspects such as menu quality, food choices, dietary diversity, supplement use, anthropometric and metabolic measures, absenteeism, and validated oxidative biomarkers when scientifically justified. Biomarker protocols ought to standardize recent work exposure: exhaled-breath-condensate 8-isoprostane levels rose following three consecutive working days, but did not show an increase after one or two days, in coal miners.²⁶ Worksite pilot interventions can employ controlled, cluster-randomized, or stepped-wedge designs when suitable, and should engage workers, dietitians, occupational physicians, industrial hygienists, safety personnel, and catering teams (Fig. 3).⁴⁶

Figure 3: Integrated workplace nutrition strategy for mining workers Click here to view Figure

Safety, Limitations, And Potential Risks Of Antioxidant Interventions

Antioxidant nutrients from common foods typically pose fewer dosage-related safety issues than concentrated supplements, but supplementation should not be assumed to be risk-free. The occupational intervention outlined above involved administering vitamin E (800 mg/day) alongside vitamin C (500 mg/day) over six months.¹⁵ The vitamin E dose exceeded typical dietary intake, yet remained below the tolerable upper intake level for U.S. adults. High doses of vitamin E may increase bleeding risk in people taking anticoagulant or antiplatelet medications because they affect platelet aggregation and vitamin K-dependent coagulation. High vitamin C intake can lead to nausea, diarrhea, and abdominal cramping, while also enhancing non-haem iron absorption. This is typically not an issue for healthy individuals, but it may exacerbate iron overload in those who are susceptible. The clinical significance of vitamin C’s suggested pro-oxidant effects remains unclear.⁴⁷ High-dose iron, copper, or manganese supplements should not be administered to metal-exposed workers unless there is a documented nutritional or clinical indication. High-dose beta-carotene should be avoided by smokers, as randomized prevention trials have indicated a rise in lung cancer incidence.⁴⁸ Excess selenium can lead to gastrointestinal, neurological, hair, and nail abnormalities, whereas excessive zinc may hinder copper absorption.⁴⁹ Wider randomized studies have not demonstrated a significant mortality advantage from antioxidant supplementation and have indicated possible harm associated with beta-carotene, vitamin A, and vitamin E in certain analyzes.⁴² Supplement use should be guided by a thorough nutritional assessment, a review of medications, verification of product quality, and monitoring for any adverse events (Table 5).

Table 5: Safety considerations for antioxidant and micronutrient interventions in mining workers

Discussion

The evidence compiled in this review indicates that oxidative stress serves as a credible integrative pathway connecting various mining exposures to respiratory and systemic biological responses; however, the robustness of the evidence varies significantly by study type. Human mining studies are mainly observational and demonstrate associations between exposure and redox-related biomarkers. In contrast, experimental studies provide mechanistic plausibility but cannot confirm clinical effects in workers. Evidence on nutritional interventions is considerably more limited and should not be regarded at the same evidentiary level as observational exposure studies.^10,18,50 The biological activity of mine dust is unlikely to be uniform because particle size, mineralogy, and geochemical composition vary across respirable fractions. Anatase, siderite, quartz, and various trace elements were linked to oxidative potential in underground coal-mine dust,⁴ indicating that gravimetric concentration alone might not fully reflect the differences in redox-active composition and biological reactivity. Coal miners who experienced higher exposure, especially those working underground and for longer durations, exhibited more significant changes in glutathione, SOD, and CAT.¹

The best evidence is for the respiratory effects. In a cross-sectional study of 145 silica-exposed miners and 45 non-silica-exposed miners, lipid peroxidation, Fenton oxidative stress, and oxidative-stress index increased. At the same time, FEV₁, FVC, FEV₁/FVC, peak expiratory flow, and FEF25–75 decreased. Lower levels of catalase, superoxide dismutase, glutathione peroxidase, and total antioxidant capacity were observed, and hematological parameters were consistent with systemic inflammation.¹¹ The cross-sectional design does not establish oxidative stress as an independent risk factor for silicosis or loss of lung function. Still, the concurrent abnormalities suggest an association among silica exposure, redox imbalance, and pulmonary dysfunction.

Human miner data reveal dose-dependent pulmonary inflammation with increasing crystalline silica burden.^9,21 At the same time, experimental studies indicate that phagocytosis of silica may lead to phagosomal destabilization and activation of the NLRP3 Inflammasome pathway. Hence, over time, there are likely to be interactions between dust dose and persistence, immune responses, smoking, previous respiratory disease, and individual susceptibility. In a 22-year follow-up of British miners and former miners, after adjusting for other factors, cumulative exposure to coal dust was inversely associated with FEV₁, FVC, and FEV₁/FVC, even among men without pneumoconiosis.⁵¹ The use of oxidative biomarkers should complement, not replace, standardized spirometry, radiological assessment, exposure assessment, and long-term pulmonary surveillance.

The biological argument extends beyond the lungs, as evidenced by systemic findings. Superoxide dismutase activity and MDA were associated with higher concentrations of toxic metals in the urine of chromite miners, particularly the extraction workers.¹⁰ In a small comparative study, lead-zinc miners’ peripheral blood lymphocytes were found to have increased ROS and oxidized glutathione, reduced glutathione and viability, and decreased mitochondrial membrane potential, with lysosomal damage.⁸ The peripheral-blood 8-OHdG levels were higher in the artisanal gold miners exposed to mercury compared to coal miners, whereas the DNA tail length, MDA, and SOD levels were higher in coal miners than in controls; the DNA tail length, MDA, and SOD levels were not different between artisanal gold miners exposed to mercury and controls.^27,33

Residual confounding and causal direction cannot be excluded in these studies, as they were observational and/or had small sample sizes. Concurrent exposures, diet, alcohol use, smoking, socioeconomic status, and age are other factors that may not have been consistently controlled and could affect redox biomarkers and disease risk. Therefore, DNA oxidation, comet assay damage, malondialdehyde, and altered antioxidant enzyme activity should be considered markers of exposure or biological response rather than indicators of cancer, heart disease, or future disability.¹²

Biomarker heterogeneity is one of the major challenges in oxidative stress studies. TBARS and MDA usually estimate lipid peroxidation, although other substances can be detected in the thiobarbituric acid-based assays.⁵² While remaining dependent on the biological matrix, analytical technique, and sampling context, F₂-isoprostanes are more specific and chemically stable products of free-radical-mediated lipid peroxidation.^30,53 The 8-isoprostane level in the exhaled breath condensate of coal miners rose after three consecutive working days but not after one or two shifts.²⁶ This result suggests that the number of consecutive shifts before collection ought to be recorded or standardized. Sampling time, recent food intake, smoking, physical workload, specimen processing, and storage should also be controlled in future studies, as these variables may affect redox measurements. A study-specific panel, which includes internal-exposure measures, oxidative-damage products, antioxidant defenses, inflammatory markers, and clinically relevant outcomes, may provide a more informative assessment than relying on a single biomarker, given the limited validation and comparability of individual assays.¹²

The difference between exposure evidence and nutritional evidence is crucial to understanding this review. Vitamin E serves as a lipid-soluble chain-breaking antioxidant, whereas vitamin C primarily functions in aqueous environments.³⁷ Additionally, manganese, copper, zinc, and selenium play a role in supporting endogenous antioxidant-enzyme systems.⁵⁴ These biochemical functions are relevant in terms of mechanism, yet they do not demonstrate clinical efficacy. The primary study on occupational supplementation reported reductions in TBARS and protein carbonyls, along with improvements in certain antioxidant measures, after administering vitamin E (800 mg/day) and vitamin C (500 mg/day). However, the study’s pre-post design, small sample sizes, varied exposures, lack of reported randomization or placebo control, high dosages, and dependence on surrogate biomarkers limit the ability to draw definitive conclusions regarding disease prevention or clinical advantages. The randomized evidence regarding antioxidant supplements has not shown a significant benefit in overall mortality and has revealed possible harm signals associated with beta-carotene, vitamin A, and vitamin E in certain analyzes.^42,55 Consequently, enhancing diet quality and addressing identified deficiencies are more justifiable than the standard practice of high-dose antioxidant supplementation in unselected mining populations.

This is particularly relevant in Saudi Arabia due to the potential for increased thermal strain from work in a hot desert environment and for exposure to mineral dust and naturally occurring radioactive materials from phosphate mining operations. The mean annual Hp(10) for 606 Saudi phosphate mine workers was 0.66 mSv, with most values less than 0.49 mSv and the highest at 3.55 mSv. The investigators suggest that both internal and external exposure be evaluated to establish a comprehensive radiation-dose baseline. However, these exposures were within the internationally reported ranges for occupational exposures.⁵⁶ Airborne radioactivity studies conducted in phosphate mining outside Saudi Arabia have shown that inhalation of radioactive dust and radon progeny can significantly contribute to the occupational dose.⁵⁷ The workers were frequently found to be dehydrated at the beginning and end of shifts, and excessive cardiovascular strain was reported in indirect evidence from Saudi construction workers.⁵⁸ Heat-related illness and dehydration are also reported from other hot environments, such as mining.^59,60 Thus, external and internal radiation evaluation, airborne dust monitoring, heat exposure management, potable water availability, appropriate work/rest cycle, and occupational health monitoring should all be part of the Saudi mining health program. The assessment of micronutrient status and nutritional quality standards can serve as supportive measures, although direct evaluation of their effectiveness in Saudi mining populations is needed.

Nutrition should be regarded as a complementary strategy that supports, rather than replaces, primary occupational prevention. Eliminating or substituting hazards and implementing engineering controls, such as wet dust suppression, enclosure, local exhaust ventilation, equipment maintenance, and exposure monitoring, are the primary methods for minimizing inhalation of coal dust, respirable crystalline silica, and other hazardous mine aerosols. When these controls fail to sufficiently limit exposure, appropriate respiratory protection is necessary.⁴³ Food-based workplace strategies have the potential to enhance dietary quality and certain cardiometabolic outcomes among general working populations. However, effects vary, and evidence for specific interventions among miners remains limited.^61–65 These methods are unable to stop particle deposition, eliminate toxic metals, or substitute for occupational controls. Future studies focused on miners should assess whole-food strategies and the targeted correction of identified deficiencies, utilizing clinically relevant nutritional, metabolic, functional, and occupational outcomes, all while ensuring consistent best-practice worker protection across the different study groups. 

This review presents certain methodological limitations. As a narrative review, it is susceptible to publication bias, selection bias, and subjective interpretation, and no formal study-level risk-of-bias tool was utilized. The literature provided a diverse range of exposure assessments, biomarker methodologies, study populations, confounder management, and outcome definitions. Older mechanistic studies were preserved for their foundational significance, while recent evidence from mining, biomarkers, and workplace nutrition was incorporated where applicable. These limitations suggest that the review should be viewed as a critical synthesis and research framework rather than a quantitative estimate of intervention efficacy. Recent advances in oxidative-stress measurement highlight the necessity for analytically specific and standardized biomarker approaches.⁶⁶

Research Gaps and Future Directions 

Most of the evidence regarding oxidative stress in mining workers is derived from cross-sectional studies, and numerous investigations feature modest sample sizes. This limitation affects causal inference and offers minimal insight into whether biomarker abnormalities can predict future disease. Prospective multicentre cohorts should measure cumulative exposure to coal dust, crystalline silica, metals, PAHs, diesel emissions, heat, and hypoxia, and link these exposures to longitudinal changes in pulmonary function, cardiometabolic health, neurological outcomes, work capacity, and clinically significant disease endpoints. Exposure assessment must include factors such as task, intensity, duration, mineralogical composition, personal monitoring, and control effectiveness, rather than depending mainly on job title or employment history.

The majority of the evidence currently available on oxidative stress in mining workers is cross-sectional, and many studies have small sample sizes, which limits the ability to draw causal conclusions and offers little insight into whether biomarker abnormalities indicate future disease. The quantitative measurement of cumulative exposure to coal dust, crystalline silica, metals, PAHs, diesel emissions, heat and hypoxia should be correlated with long-term changes in pulmonary function, cardiometabolic health, neurological outcomes and work capacity in prospective multicenter cohorts. Exposure assessment should consider task, intensity, duration, mineralogical composition, personal monitoring and control effectiveness, rather than just job titles and employment history.

Standardizing biomarkers is an additional priority. Current research employs a variety of measures for MDA, TBARS, glutathione, antioxidant enzymes, DNA damage, and total antioxidant capacity, highlighting significant differences in analytical specificity and comparability.^12,66,67 Future studies should employ prespecified, study-specific panels that integrate internal-exposure measures, chemically specific oxidative-damage products, antioxidant defenses, inflammatory markers, and clinically relevant outcomes. It is essential that the shift sequence, sampling time, recent diet, smoking habits, physical workload, specimen processing, and storage are either standardized or clearly documented. Conducting repeated measurements over successive shifts and extending the follow-up period may aid in differentiating between transient adaptive responses and persistent redox disturbances.⁶⁸

The consistency of biomarkers is another major concern. Most of the heterogeneous assays used in existing studies for MDA, TBARS, glutathione, antioxidant enzymes, DNA damage, and total antioxidant capacity are not validated and are not comparable across studies.^12,67 Study-specific panels for internal exposure measurements, chemically specific oxidative damage products, antioxidant defenses, inflammatory markers, and clinical outcomes should be combined in future research. Shift sequence, sampling time, recent diet, smoking, physical workload, specimen processing and storage should be standardized or well documented. The longer follow-up and repeated measurements over successive shifts might be able to distinguish reversible from persistent redox disturbance.⁶⁸

Research on nutritional interventions specific to miners should advance past uncontrolled biomarker studies. Where possible, sufficiently powered randomized controlled trials, cluster-randomized trials, or stepped-wedge trials should assess whole-food programs, workplace catering reforms, and targeted corrections of identified deficiencies. Trials ought to clearly define baseline nutritional status, adherence, adverse events, medication use, occupational exposure intensity, and clinically significant pulmonary, metabolic, functional, quality-of-life, and occupational outcomes. Follow-up should also be long enough to assess whether benefits or harms persist. High-dose supplementation should be used with caution, especially among smokers or individuals exposed to significant levels of metal.⁶⁹ Multicentre studies ought to intentionally incorporate women, migrant workers, and populations that have been less studied, such as those in Saudi Arabia.^70,71 All study groups must maintain access to equivalent best-practice exposure controls, as nutrition cannot substitute for dust suppression, ventilation, heat management, respiratory protection, or occupational surveillance.

The reviewed literature showed very few controlled nutritional interventions, specific to a particular miner. Trials should measure nutritional status, adherence, adverse events, medication use, and clinically important pulmonary, metabolic, functional, and occupational outcomes, and assess whole-food programs, workplace catering reform, and targeted correction of documented deficiencies. The use of high doses of supplementation on a whim, particularly in smokers or workers with high exposure to metals, is not recommended.⁶⁹ It is important to specifically include women, migrant workers, and under-researched populations, such as Saudi Arabia, in multicenter research.^70,71 All study groups should receive comparable best-practice exposure control measures, as nutrition cannot replace dust suppression, ventilation, heat control, respiratory protection, and/or occupational surveillance.

Conclusion

Mining exposures are regularly linked to disruptions in redox-related biomarkers and to both pulmonary and systemic biological effects. However, the existing human evidence is mainly observational, varied, and constrained by non-standardized biomarker methods. Evidence for nutritional interventions is considerably less robust: controlled trials specific to minerals are limited, and the primary evidence for supplementation relies on surrogate biomarkers instead of clinical outcomes. Current evidence does not demonstrate that antioxidant supplements prevent or treat mining-related diseases and does not endorse routine high-dose supplementation in unselected workers. Adequate dietary quality and correction of documented deficiencies may support general health; however, workplace nutrition should complement, rather than replace, dust suppression, ventilation, respiratory protection, heat management, exposure monitoring, and medical surveillance. Future research should focus on prospective multicentre cohorts and well-powered controlled nutrition trials that utilize standardized oxidative-stress measures, thorough exposure assessment, and clinically significant long-term outcomes.

Acknowledgment

The authors extend their appreciation to Northern Border University, Saudi Arabia, for supporting this work through project number (NBU-CRP-2026-2043).

Funding Sources

The author(s) received no financial support for the research, authorship, and/or publication of this article 

Conflict Of Interest

The authors do not have any conflict of interest.

Data Availability Statement

All the information presented was obtained from previously published studies and publicly available databases with proper citations. The corresponding author can provide any datasets used for this study upon request.

Ethics Statement

This research did not involve human participants, animal subjects, or any material that requires ethical approval.

Informed Consent Statement

This study did not involve human participants, and therefore, informed consent was not required.

Clinical Trial Registration

This research does not involve any clinical trials.

Permission to Reproduce Material from Other Sources

Not Applicable.

Author Contributions

• Abida Khan: Conceptualization, Data collection, Critical Analysis, Manuscript drafting, and Review and editing.
• Howayada Mahany Mostafa: Data collection, Manuscript drafting, Critical Analysis, and Review and editing
• Syed Raziuddin Quadri: Data collection, Manuscript drafting, Review and editing.
• Mohd Imran: Conceptualization, Supervision, Critical Analysis, Review, and editing. 

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Abbreviation

8-OHdG  –          8-Hydroxy-2′-deoxyguanosine

8-oxodG   –        8-Oxo-2′-deoxyguanosine

Alu(Yb8)   –      Alu Yb8 repetitive element

CAT –                   Catalase

Cu/Zn-SOD  –  Copper/Zinc Superoxide Dismutase

DNA –                  Deoxyribonucleic Acid

FEF25–75 –       Forced Expiratory Flow between 25% and 75% of Forced Vital Capacity

FEV₁ –                 Forced Expiratory Volume in One Second

FEV₁/FVC –      Ratio of Forced Expiratory Volume in One Second to Forced Vital Capacity

F₂-isoprostanes –  F₂-Isoprostanes

FVC –                  Forced Vital Capacity

GPx –                  Glutathione Peroxidase

GR –                    Glutathione Reductase

GSH –                  Reduced Glutathione

GSH: GSSG ratio –  Ratio of Reduced Glutathione to Oxidized Glutathione

GSSG –                 Oxidized Glutathione

GST –                   Glutathione-S-Transferase

Hp(10) –              Personal Dose Equivalent at a Tissue Depth of 10 mm

LINE1 –               Long Interspersed Nuclear Element-1

MDA –                 Malondialdehyde

MEDLINE –       Medical Literature Analysis and Retrieval System Online

MEF –                 Maximum Expiratory Flow

Mn-SOD –          Manganese Superoxide Dismutase

NLRP3 –            NOD-, LRR- and Pyrin Domain-Containing Protein 3

PAHs –               Polycyclic Aromatic Hydrocarbon

PEF –                 Peak Expiratory Flow

PPE –                 Personal Protective Equipment

RNS –                Reactive Nitrogen Species

ROS –                Reactive Oxygen Species

SOD –                Superoxide Dismutase

TAC –                Total Antioxidant Capacity

TBARS –           Thiobarbituric Acid-Reactive Substances

Cd –                   Cadmium

Cr –                    Chromium

Cu –                   Copper

Hg –                  Mercury

Mn –                 Manganese

Ni –                   Nickel

Pb –                  Lead

Zn –                  Zinc

mSv –        Millisievert