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MINI REVIEW article

Front. Nutr., 14 July 2023
Sec. Food Chemistry
This article is part of the Research Topic Nutritional Toxicity: Physiology, Nutrition, and Human Health View all 13 articles

Arsenic in brown rice: do the benefits outweigh the risks?

  • 1Peter O’Donnell Jr. School of Public Health, University of Texas Southwestern Medical Center, Dallas, TX, United States
  • 2Fay W. Boozman College of Public Health, University of Arkansas for Medical Sciences, Little Rock, AR, United States

Brown rice has been advocated for as a healthier alternative to white rice. However, the concentration of arsenic and other pesticide contaminants is greater in brown rice than in white. The potential health risks and benefits of consuming more brown rice than white rice remain unclear; thus, mainstream nutritional messaging should not advocate for brown rice over white rice. This mini-review aims to summarize the most salient concepts related to dietary arsenic exposure with emphasis on more recent findings and provide consumers with evidence of both risks and benefits of consuming more brown rice than white rice. Despite risk-benefit assessments being a challenging new frontier in nutrition, researchers should pursue an assessment to validate findings and solidify evidence. In the interim, consumers should be cognizant that the dose of arsenic exposure determines its toxicity, and brown rice contains a greater concentration of arsenic than white rice.

Introduction

In recent years, gluten-free, dairy-free, and plant-based dieting has increased in popularity, and rice is a common substitute. The potential health risks and benefits of consuming more brown rice than white rice remain unclear. Despite this, brown rice is often advocated as a healthier alternative to white rice in mainstream diet and nutritional messaging. Evidence of any protective effect of consuming more brown rice than white is limited.

Even though in-vitro and animal studies using nutrients and fiber extracted from brown rice have demonstrated improved cardiovascular function and prevention of heart diseases (15), these studies fail to utilize the whole grain of brown rice. Additionally, Sun et al. (6) found that when compared to white rice intake, brown rice intake reduced the risk of type 2 diabetes by 16%. The study, however, lacked diversity and included a homogenous population of European descent health professionals.

Current literature widely includes animal studies and primarily examines the benefits of consuming whole grains, not specifically brown rice. Other study limitations fail to provide solid evidence for the health benefits of consuming brown rice over white rice. There is a clear lack of research focusing on human consumption of brown rice that includes a risk-benefit approach. Risk-benefit assessment of foods is a challenging new frontier in food safety research. The assessment estimates human health benefits and risks following exposure (or lack thereof) to a particular food or food component and integrates them into comparable measures (79).

What might continue diminishing the evidence between brown rice and its human health benefits? Brown rice contains a greater arsenic concentration than white rice, and the human health risks associated with dietary arsenic exposure are well-established.

Dietary exposure to arsenic

Arsenic is ubiquitous in the environment and is a global public health concern. Arsenic is a well-known carcinogenic, mutagenic, and toxic environmental element that occurs as inorganic arsenic and organoarsenical compounds (10). Arsenic can be found in food, water, soil, and airborne particles. Inorganic forms of arsenic are found in the environment dissolved in water, and human exposure occurs through drinking water. Additionally, diet is an alternative source of exposure through the consumption of plant-based foods such as wheat, rice, and vegetables grown in contaminated soil and animal products such as dairy, milk, and fish exposed to contaminated feed. Even soil from organic farms can have remnants of arsenic due to historical pesticide use.

Because of the rapid globalization in the food trade, the ingestion of arsenic through rice consumption is not limited to a regional issue but a worldwide health concern (11, 12). A study of more than 204 rice samples sold in the U.S. found that rice grown in certain Southern states, which accounts for more than 47% of the U.S. market, had the highest arsenic content compared to the rice imported from Asia or grown in California (13). A 2017 study estimated Americans’ inorganic arsenic exposures from drinking water and rice. It concluded that rice consumption might account for as much inorganic arsenic exposure as drinking water in some U.S. populations (14).

The U.S. Environmental Protection Agency set a limit for total arsenic in drinking water at 10 parts per billion (ppb). However, no such limit exists for food or other beverages. Thus, rice can contain levels of inorganic arsenic that surpass the limit set for arsenic in drinking water. In 2014, a Consumer Reports analysis of the U.S. Food and Drug Administration (FDA) data on 656 rice products confirmed the worrisome levels of arsenic exposure from white and brown rice. In rice, inorganic arsenic is found in the two outer layers of the grain (i.e., bran and germ), and the bran and germ are removed to refine the grain into white rice. Thus, a greater concentration of arsenic is found in brown rice than in white rice. In the previously cited Consumer Reports study, brown rice contained 80 percent more inorganic arsenic on average than white rice of the same type (15).

In response to concerns raised by the public, the FDA Center for Food Safety and Applied Nutrition conducted an assessment based on the existing evidence of health risks from inorganic arsenic in rice and products that contain rice (16). The investigation concluded that the average concentrations of inorganic arsenic are 92 ppb in white rice, 154 ppb in brown rice, 104 ppb in infants’ dry white rice cereal, and 119 ppb in infants’ dry-brown rice cereal. The data demonstrated that inorganic arsenic concentration is 1.5 times higher in brown rice than in white rice. The expert panel concluded that the risk of exposure and associated health condition(s) increases proportionally with consumption and depends on the type of rice consumed. Notably, the FDA assessment focused on lung and bladder cancer. The expert panel concluded that cancer cases would have increased by 148.6% if rice consumption increased from less than one serving per day, the current level, to precisely one serving per day (16). Although none of the products analyzed in the Consumer Reports study reached the acute toxicity level, the health effects of long-term low-dose exposure are unclear. According to the U.S. FDA, the adverse health effects of arsenic exposure depend on various factors, such as the type of arsenic (organic or inorganic), the level of exposure, and the age of the person exposed to the arsenic. Many studies have linked arsenic exposure to cancers, cardiovascular disease, diabetes mellitus, hypertension, and obesity (17, 18).

Arsenic exposure and disease

Various studies have demonstrated that pregnant females, fetuses, and neonates suffer adverse pregnancy outcomes when exposed to arsenic (1923). In utero, inorganic arsenic exposure was positively associated with DNA damage in offspring (24). Recent health risk assessments reported that the consumption of arsenic-containing rice and rice-based foods (e.g., cereals, cakes, and crackers) led to increased cancer risks, especially in subpopulations of infants and children (2529).

In humans, inorganic arsenic compounds are converted to trivalent arsenic (AsIII) and pentavalent arsenate (AsV). AsV is rapidly converted to AsIII. AsIII species are more toxic and bioactive than AsV species, both because of the greater chemical reactivity of AsIII and because AsIII enters cells more easily (30). Both arsenic species coexist in drinking water with varying toxicity (31). According to the International Agency for Research on Cancer (IARC), there is sufficient evidence in humans for the carcinogenicity of mixed exposure to inorganic arsenic compounds, including arsenic trioxide, arsenite, and arsenate. Exposure to arsenic stimulates epigenetic disruption in various cellular processes, which can cause cancer. Presently, three modes (i.e., chromosomal abnormality, oxidative stress, and altered growth factors) of arsenic carcinogenesis have a degree of positive evidence, both in experimental systems (animal and human cells) and in human tissues (3234). The IARC concludes that different inorganic arsenic species should be considered carcinogenic independent of the mechanisms of carcinogenic action and independent of which metabolites are the ultimate carcinogen (30).

Chronic arsenic exposure through consuming certain foods and contaminated water has been associated with an increased risk of prostate, lung, bladder, pancreatic, and skin cancer (31, 3540). According to the U.S. National Cancer Institute, cancers of the digestive tract, liver, kidney, and lymphatic and hematopoietic systems have also been linked to arsenic exposure. Additionally, arsenic trioxide (As2O3) treatment in human fibroblasts was shown to disrupt the normal function of the DNA repair pathway and increase genomic instability (24), such that women carrying specific BRCA-1 mutations (e.g., 5382insC, C61G, and 4153delA) were found to be at higher risk of breast cancer with increased arsenic exposure (41).

Arsenic is one of many environmental pollutants linked to metabolic syndrome development (17, 18, 42). Metabolic risk factors that lead to a diagnosis of arsenic-induced metabolic syndrome include having a large waistline, high blood pressure, elevated fasting blood sugar, high triglyceride level, and low HDL cholesterol. Those risk factors are identical to the ones for cardiovascular diseases.

Epidemiological studies have shown that the cardiovascular system is susceptible to long-term ingestion of arsenic (43). Noticeable effects include hypertension and increased cardiovascular disease mortality (43). A growing body of literature suggests that DNA methylation, one of the most frequently researched epigenetic mechanisms, is associated with various outcomes in response to exposure to heavy metals like arsenic (4447). A recent study proposed epigenetic dysregulation as a critical arsenic-related cardiovascular disease (CVD) mechanism. Researchers conducted a mediation analysis to assess the potential role of DNA methylation on arsenic-related CVD. Results supported that blood DNA methylation influences arsenic-related CVD, and the results were replicated in a mouse model and three independent and diverse human cohorts (48).

In addition, arsenic exposure is also suspected to be related to obesity (24, 49). We recently found a significant dose–response relationship between arsenic concentration and obesity among 270 postmenopausal women randomly selected from a study cohort where most rice is produced (50). Furthermore, we also found a significantly positive association between weight gain velocity and salivary arsenic concentration in the same study. The mechanism for arsenic exposure and obesity is unclear. Arsenic upregulates the cytokine IL-6 expression in various cell types (51). IL-6, a pro-inflammatory cytokine and an anti-inflammatory myokine, is hypothesized to increase the amount of free fatty acids in the body, thus increasing obesity. Another explanation involves regulating glucose uptake by the glucose transporter 4 protein (GLUT4) in adipose and skeletal muscles (52). A recent study determined that low-dose exposure to arsenic for 8 weeks decreased GLUT4 expression (53). When GLUT4 is silenced, the glucose is not effectively transported into the cell. Research has further identified that steady-state glucose homeostasis dysregulations are due to arsenic exposure (54). Although the mechanism remained largely unknown, patterns of dyslipidemia influenced by arsenic have been identified (55).

Conclusion

There is a clear lack of research focusing on human consumption of brown rice that includes a risk-benefit approach. The fact that brown rice contains more arsenic than white rice cannot be denied, and the human health risks associated with dietary arsenic exposure are well-established. Health effects of arsenic exposure depend on various factors, such as the type of arsenic (organic or inorganic), the level of exposure, and the age of the person exposed to the arsenic. Arsenic exposure has been associated with cancers, cardiovascular disease, diabetes mellitus, hypertension, and obesity. Despite risk-benefit assessment of foods being a challenging new frontier in food safety research, future studies should include an assessment to validate findings and solidify evidence. In the interim, consumers should be cognizant that the dose of arsenic exposure determines its toxicity, and brown rice contains a greater concentration of arsenic than white rice.

Author contributions

LS drafted the manuscript. LS, T-CC, and SO’C reviewed and completed the manuscript. All authors contributed to the article and approved the submitted version.

Conflict of interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Publisher’s note

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

Abbreviations

AsIII, Trivalent arsenic; As2O3, Arsenic trioxide; AsV, Pentavalent arsenate; FDA U.S., Food and Drug Administration; GLUT4, Glucose transporter 4 protein; HDL, High-density lipoprotein; U.S., The United States of America.

References

1. Kim, JY, Do, MH, and Lee, SS. The effects of a mixture of brown and black rice on lipid profiles and antioxidant status in rats. Ann Nutr Metab. (2006) 50:347–53. doi: 10.1159/000094298

PubMed Abstract | CrossRef Full Text | Google Scholar

2. Petchdee, S, Laosripaiboon, W, and Jarussophon, N. Cardiac protection of germinated brown rice extract in rabbit model of chronic myocardial infarction. Translational. Anim Sci. (2020) 4:txaa067. doi: 10.1093/tas/txaa067

PubMed Abstract | CrossRef Full Text | Google Scholar

3. Yen, H-W, Lin, H-L, Hao, C-L, Chen, F-C, Chen, C-Y, Chen, J-H, et al. Effects of pre-germinated brown rice treatment high-fat diet-induced metabolic syndrome in C57BL/6J mice. Biosci Biotechnol Biochem. (2017) 81:979–86. doi: 10.1080/09168451.2017.1279848

PubMed Abstract | CrossRef Full Text | Google Scholar

4. Zhao, R, Ghazzawi, N, Wu, J, Le, K, Li, C, Moghadasian, MH, et al. Germinated brown rice attenuates atherosclerosis and vascular inflammation in low-density lipoprotein receptor-knockout mice. J Agric Food Chem. (2018) 66:4512–20. doi: 10.1021/acs.jafc.8b00005

PubMed Abstract | CrossRef Full Text | Google Scholar

5. Petchdee, S, Laosripaiboon, W, Jarussophon, N, and Kumphune, S. Cardio-protective effects of germinated Brown Rice extract against myocardial ischemia reperfusion injury. High Blood Pressure Cardiovasc Prevent Off J Italian Soc Hypertension. (2020) 27:251–8. doi: 10.1007/s40292-020-00378-x

PubMed Abstract | CrossRef Full Text | Google Scholar

6. Sun, Q, Spiegelman, D, van Dam, RM, et al. White Rice, Brown Rice, and risk of type 2 diabetes in U.S. men and women. Arch Intern Med. (2010) 170:961–9. doi: 10.1001/archinternmed.2010.109

PubMed Abstract | CrossRef Full Text | Google Scholar

7. Assunção, R, Pires, S, and Nauta, M. Risk-benefit assessment of foods. EFSA J. (2019) 17:e170917. doi: 10.2903/j.efsa.2019.e170917

PubMed Abstract | CrossRef Full Text | Google Scholar

8. Boué, G, Guillou, S, Antignac, JP, Bizec, B, and Membré, JM. Public health risk-benefit assessment associated with food consumption – a review. Eur J Nutr Food Safety. (2015) 5:32–58. doi: 10.9734/ejnfs/2015/12285

CrossRef Full Text | Google Scholar

9. Pires, SM, Boué, G, Boobis, A, Eneroth, H, Hoekstra, J, Membré, JM, et al. Risk-benefit assessment of foods: key findings from an international workshop. Food Res Int. (2019) 116:859–69. doi: 10.1016/j.foodres.2018.09.021

CrossRef Full Text | Google Scholar

10. D’Amore, T, Miedico, O, Pompa, C, Preite, C, Iammarino, M, and Nardelli, V. Characterization and quantification of arsenic species in foodstuffs of plant origin by HPLC/ICP-MS. Life. (2023) 13:511. doi: 10.3390/life13020511

PubMed Abstract | CrossRef Full Text | Google Scholar

11. Islam, S, Rahman, MM, Rahman, MA, and Naidu, R. Inorganic arsenic in rice and rice-based diets: health risk assessment. Food Control. (2017) 82:196–202. doi: 10.1016/j.foodcont.2017.06.030

CrossRef Full Text | Google Scholar

12. Kumarathilaka, P, Seneweera, S, Meharg, A, and Bundschuh, J. Arsenic accumulation in rice (Oryza sativa L.) is influenced by environment and genetic factors. Sci Total Environ. (2018) 642:485–96. doi: 10.1016/j.scitotenv.2018.06.030

PubMed Abstract | CrossRef Full Text | Google Scholar

13. Zavala, YJ, and Duxbury, JM. Arsenic in rice: I. estimating normal levels of total arsenic in rice grain. Environ Sci Technol. (2008) 42:3856–60. doi: 10.1021/es702747y

PubMed Abstract | CrossRef Full Text | Google Scholar

14. Mantha, M, Yeary, E, Trent, J, Creed, PA, Kubachka, K, Hanley, T, et al. Estimating inorganic arsenic exposure from U.S. Rice and Total water intakes. Environ Health Perspect. (2017) 125:057005. doi: 10.1289/EHP418

PubMed Abstract | CrossRef Full Text | Google Scholar

15. Consumer Reports Food Safety and Sustainability Center. (2014). Report: analysis of arsenic in Rice and other grains. Available at: https://advocacy.consumerreports.org/wp-content/uploads/2019/05/CR_FSASC_Arsenic_Analysis_Nov2014.pdf

Google Scholar

16. Center for Food Safety and Applied Nutrition—U.S. Food and Drug Administration. (2016). Risk Assessment Report: Arsenic in Rice and Rice Products. Available at: http://www.fda.gov/Food/FoodScienceResearch/RiskSafetyAssessment/default.htm

Google Scholar

17. Jeon, JY, Ha, KH, and Kim, DJ. New risk factors for obesity and diabetes: environmental chemicals. J Diabetes Investig. (2015) 6:109–11. doi: 10.1111/jdi.12318

PubMed Abstract | CrossRef Full Text | Google Scholar

18. Lin, H-C, Huang, Y-K, Shiue, H-S, Chen, L-S, Choy, C-S, Huang, S-R, et al. Arsenic methylation capacity and obesity are associated with insulin resistance in obese children and adolescents. Food Chem Toxicol. (2014) 74:60–7. doi: 10.1016/j.fct.2014.08.018

PubMed Abstract | CrossRef Full Text | Google Scholar

19. Farzan, SF, Karagas, MR, and Chen, Y. In utero and early life arsenic exposure in relation to long-term health and disease. Toxicol Appl Pharmacol. (2013) 272:384–90. doi: 10.1016/j.taap.2013.06.030

PubMed Abstract | CrossRef Full Text | Google Scholar

20. Milton, AH, Hussain, S, Akter, S, Rahman, M, Mouly, TA, and Mitchell, K. A review of the effects of chronic arsenic exposure on adverse pregnancy outcomes. Int J Environ Res Public Health. (2017) 14:556. doi: 10.3390/ijerph14060556

PubMed Abstract | CrossRef Full Text | Google Scholar

21. Milton, AH, Smith, W, Rahman, B, Hasan, Z, Kulsum, U, Dear, K, et al. Chronic arsenic exposure and adverse pregnancy outcomes in Bangladesh. Epidemiology. (2005) 16:82–6. doi: 10.1097/01.ede.0000147105.94041.e6

CrossRef Full Text | Google Scholar

22. Rahman, A, Vahter, M, Smith, AH, Nermell, B, Yunus, M, El Arifeen, S, et al. Arsenic exposure during pregnancy and size at birth: a prospective cohort study in Bangladesh. Am J Epidemiol. (2009) 169:304–12. doi: 10.1093/aje/kwn332

PubMed Abstract | CrossRef Full Text | Google Scholar

23. Ronco, AM, Gutierrez, Y, Gras, N, Muñoz, L, Salazar, G, and Llanos, MN. Lead and arsenic levels in women with different body mass composition. Biol Trace Elem Res. (2010) 136:269–78. doi: 10.1007/s12011-009-8546-z

PubMed Abstract | CrossRef Full Text | Google Scholar

24. Peremartí, J, Ramos, F, Marcos, R, and Hernández, A. Arsenic exposure disrupts the normal function of the FA/BRCA repair pathway. Toxicol Sci Off J Soc Toxicol. (2014) 142:93–104. doi: 10.1093/toxsci/kfu159

PubMed Abstract | CrossRef Full Text | Google Scholar

25. Fakhri, Y, Bjørklund, G, Bandpei, AM, Chirumbolo, S, Keramati, H, Hosseini Pouya, R, et al. Concentrations of arsenic and lead in rice (Oryza sativa L.) in Iran: a systematic review and carcinogenic risk assessment. Food Chem Toxicol. (2018) 113:267–77. doi: 10.1016/j.fct.2018.01.018

PubMed Abstract | CrossRef Full Text | Google Scholar

26. Islam, S, Rahman, MM, Islam, MR, and Naidu, R. Arsenic accumulation in rice: consequences of rice genotypes and management practices to reduce human health risk. Environ Int. (2016) 96:139–55. doi: 10.1016/j.envint.2016.09.006

PubMed Abstract | CrossRef Full Text | Google Scholar

27. Lin, K, Lu, S, Wang, J, and Yang, Y. The arsenic contamination of rice in Guangdong Province, the most economically dynamic provinces of China: arsenic speciation and its potential health risk. Environ Geochem Health. (2015) 37:353–61. doi: 10.1007/s10653-014-9652-1

PubMed Abstract | CrossRef Full Text | Google Scholar

28. Rahman, MA, Rahman, MM, Reichman, SM, Lim, RP, and Naidu, R. Arsenic speciation in Australian-grown and imported rice on sale in Australia: implications for human health risk. J Agric Food Chem. (2014) 62:6016–24. doi: 10.1021/jf501077w

PubMed Abstract | CrossRef Full Text | Google Scholar

29. Sofuoglu, SC, Güzelkaya, H, Akgül, Ö, Kavcar, P, Kurucaovalı, F, and Sofuoglu, A. Speciated arsenic concentrations, exposure, and associated health risks for rice and bulgur. Food Chem Toxicol. (2014) 64:184–91. doi: 10.1016/j.fct.2013.11.029

PubMed Abstract | CrossRef Full Text | Google Scholar

30. IARC—International Agency for Research on Cancer (2012). Arsenic, metals, fibres, and dusts. IARC monographs on the evaluation of carcinogenic risks to humans ; World Health Organization WHO-Press: Lyon, France; 100C

Google Scholar

31. Sorg, TJ, Chen, ASC, and Wang, L. Arsenic species in drinking water wells in the USA with high arsenic concentrations. Water Res. (2014) 48:156–69. doi: 10.1016/j.watres.2013.09.016

PubMed Abstract | CrossRef Full Text | Google Scholar

32. Bhattacharjee, P, Banerjee, M, and Giri, AK. Role of genomic instability in arsenic-induced carcinogenicity. Rev Environ Int. (2013) 53:29–40. doi: 10.1016/j.envint.2012.12.004

PubMed Abstract | CrossRef Full Text | Google Scholar

33. Kitchin, KT. Recent advances in arsenic carcinogenesis: modes of action, animal model systems, and methylated arsenic metabolites. Toxicol Appl Pharmacol. (2001) 172:249–61. doi: 10.1006/taap.2001.9157

PubMed Abstract | CrossRef Full Text | Google Scholar

34. Tong, D, Ortega, J, Kim, C, Huang, J, Gu, L, and Li, G-M. Arsenic inhibits DNA mismatch repair by promoting EGFR expression and PCNA phosphorylation. J Biol Chem. (2015) 290:14536–41. doi: 10.1074/jbc.M115.641399

PubMed Abstract | CrossRef Full Text | Google Scholar

35. Ayotte, JD, Belaval, M, Olson, SA, Burow, KR, Flanagan, SM, Hinkle, SR, et al. Factors affecting temporal variability of arsenic in groundwater used for drinking water supply in the United States. Sci Total Environ. (2015) 505:1370–9. doi: 10.1016/j.scitotenv.2014.02.057

PubMed Abstract | CrossRef Full Text | Google Scholar

36. Brambila, EM, Achanzar, WE, Qu, W, Webber, MM, and Waalkes, MP. Chronic arsenic-exposed human prostate epithelial cells exhibit stable arsenic tolerance: mechanistic implications of altered cellular glutathione and glutathione S-transferase. Toxicol Appl Pharmacol. (2002) 183:99–107. doi: 10.1006/taap.2002.9468

PubMed Abstract | CrossRef Full Text | Google Scholar

37. García-Esquinas, E, Pollán, M, Umans, JG, Francesconi, KA, Goessler, W, Guallar, E, et al. Arsenic exposure and cancer mortality in a U.S.-based prospective cohort: the strong heart study. Cancer epidemiology, Biomarkers & Prevention: a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive. Oncology. (2013) 22:1944–53. doi: 10.1158/1055-9965.EPI-13-0234-T

PubMed Abstract | CrossRef Full Text | Google Scholar

38. Lewis, DR, Southwick, JW, Ouellet-Hellstrom, R, Rench, J, and Calderon, RL. Drinking water arsenic in Utah: a cohort mortality study. Environ Health Perspect. (1999) 107:359–65. doi: 10.1289/ehp.99107359

PubMed Abstract | CrossRef Full Text | Google Scholar

39. Sanchez, TR, Perzanowski, M, and Graziano, JH. Inorganic arsenic and respiratory health, from early life exposure to sex-specific effects: a systematic review. Environ Res. (2016) 147:537–55. doi: 10.1016/j.envres.2016.02.009

PubMed Abstract | CrossRef Full Text | Google Scholar

40. Yang, Y, McDonald, AC, Wang, X, Pan, Y, and Wang, M. Arsenic exposures and prostate cancer risk: a multilevel meta-analysis. J Trace Elem Med Biol Organ Soc Miner Trace Elements. (2022) 72:126992. doi: 10.1016/j.jtemb.2022.126992

PubMed Abstract | CrossRef Full Text | Google Scholar

41. Muszyńska, M, Jaworska-Bieniek, K, Durda, K, Sukiennicki, G, Gromowski, T, and Jakubowska, A. Arsenic (as) and breast cancer risk. Hereditary Cancer Clin Practice. (2012) 10:A8. doi: 10.1186/1897-4287-10-S4-A8

CrossRef Full Text | Google Scholar

42. Steinmaus, C, Castriota, F, Ferreccio, C, Smith, AH, Yuan, Y, Liaw, J, et al. Obesity and excess weight in early adulthood and high risks of arsenic-related cancer in later life. Environ Res. (2015) 142:594–601. doi: 10.1016/j.envres.2015.07.021

PubMed Abstract | CrossRef Full Text | Google Scholar

43. National Research Council Subcommittee to Update the Arsenic in Drinking Water, R. Arsenic in drinking water: 2001 update. U.S.: National Academies Press (2001).

Google Scholar

44. Bozack, AK, Domingo-Relloso, A, Haack, K, Gamble, MV, Tellez-Plaza, M, Umans, JG, et al. Locus-specific differential DNA methylation and urinary arsenic: an epigenome-wide association study in blood among adults with low-to-moderate arsenic exposure. Environ Health Perspect. (2020) 128:67015. doi: 10.1289/EHP6263

PubMed Abstract | CrossRef Full Text | Google Scholar

45. Cardenas, A, Koestler, DC, Houseman, EA, Jackson, BP, Kile, ML, Karagas, MR, et al. Differential DNA methylation in umbilical cord blood of infants exposed to mercury and arsenic in utero. Epigenetics. (2015) 10:508–15. doi: 10.1080/15592294.2015.1046026

PubMed Abstract | CrossRef Full Text | Google Scholar

46. Green, BB, Karagas, MR, Punshon, T, Jackson, BP, Robbins, DJ, Houseman, EA, et al. Epigenome-wide assessment of DNA methylation in the placenta and arsenic exposure in the New Hampshire birth cohort study (USA). Environ Health Perspect. (2016) 124:1253–60. doi: 10.1289/ehp.1510437

PubMed Abstract | CrossRef Full Text | Google Scholar

47. Koestler, DC, Avissar-Whiting, M, Houseman, EA, Karagas, MR, and Marsit, CJ. Differential DNA methylation in umbilical cord blood of infants exposed to low levels of arsenic in utero. Environ Health Perspect. (2013) 121:971–7. doi: 10.1289/ehp.1205925

PubMed Abstract | CrossRef Full Text | Google Scholar

48. Domingo-Relloso, A, Makhani, K, Riffo-Campos, AL, Tellez-Plaza, M, Klein, KO, Subedi, P, et al. Arsenic exposure, blood DNA methylation, and cardiovascular disease. Circ Res. (2022) 131:e51–69. doi: 10.1161/CIRCRESAHA.122.320991

PubMed Abstract | CrossRef Full Text | Google Scholar

49. Chou, W-C, Chung, Y-T, Chen, H-Y, Wang, C-J, Ying, T-H, Chuang, C-Y, et al. Maternal arsenic exposure and DNA damage biomarkers, and the associations with birth outcomes in a general population from Taiwan. PLoS One. (2014) 9:e86398. doi: 10.1371/journal.pone.0086398

PubMed Abstract | CrossRef Full Text | Google Scholar

50. Stahr, S, Chiang, T, Bauer, MA, Runnells, GA, Rogers, LJ, and Joseph Su, L. Low-level environmental heavy metals are associated with obesity among postmenopausal women in a southern state. Exposure Health. (2021) 13:269–80. doi: 10.1007/s12403-020-00381-6

PubMed Abstract | CrossRef Full Text | Google Scholar

51. Agrawal, S, Bhatnagar, P, and Flora, SJS. Changes in tissue oxidative stress, brain biogenic amines and acetylcholinesterase following co-exposure to lead, arsenic and mercury in rats. Food Chem Toxicol. (2015) 86:208–16. doi: 10.1016/j.fct.2015.10.013

PubMed Abstract | CrossRef Full Text | Google Scholar

52. Rüegg, J, Cai, W, Karimi, M, Kiss, NB, Swedenborg, E, Larsson, C, et al. Epigenetic regulation of glucose transporter 4 by estrogen receptor β. Molecul Endocrinol Baltimore. (2011) 25:2017–28. doi: 10.1210/me.2011-1054

PubMed Abstract | CrossRef Full Text | Google Scholar

53. Farkhondeh, T, Samarghandian, S, and Azimi-Nezhad, M. The role of arsenic in obesity and diabetes. J Cell Physiol. (2019) 234:12516–29. doi: 10.1002/jcp.28112

PubMed Abstract | CrossRef Full Text | Google Scholar

54. Kirkley, AG, Carmean, CM, Ruiz, D, Ye, H, Regnier, SM, Poudel, A, et al. Arsenic exposure induces glucose intolerance and alters global energy metabolism. Am J Physiol Regul Integr Comp Physiol. (2018) 314:R294–303. doi: 10.1152/ajpregu.00522.2016

PubMed Abstract | CrossRef Full Text | Google Scholar

55. Afolabi, OK, Wusu, AD, Ogunrinola, OO, Abam, EO, Babayemi, DO, Dosumu, OA, et al. Arsenic-induced dyslipidemia in male albino rats: comparison between trivalent and pentavalent inorganic arsenic in drinking water. BMC Pharmacol Toxicol. (2015) 16:15. doi: 10.1186/s40360-015-0015-z

PubMed Abstract | CrossRef Full Text | Google Scholar

Keywords: arsenic, exposure, brown rice, cancer, obesity, cardiovascular health

Citation: Su LJ, Chiang T-C and O’Connor SN (2023) Arsenic in brown rice: do the benefits outweigh the risks? Front. Nutr. 10:1209574. doi: 10.3389/fnut.2023.1209574

Received: 20 April 2023; Accepted: 26 June 2023;
Published: 14 July 2023.

Edited by:

Misha Vrolijk, Maastricht University, Netherlands

Reviewed by:

Marco Iammarino, Experimental Zooprophylactic Institute of Puglia and Basilicata (IZSPB), Italy

Copyright © 2023 Su, Chiang and O’Connor. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Lihchyun Joseph Su, TGloY2h5dW4uU3VAVVRTb3V0aHdlc3Rlcm4uZWR1

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