modulating our exposure and elimination of chemicals

Epigenetics infers that nutrients can and do interact with the human genome to change molecular pathways that can become disrupted, eventually leading to risk of developing a chronic disease (El-Sohemy, 2007). Genetic polymorphisms have a way of affecting metabolism of dietary factors that, in turn, affect genetic expression involved in many metabolic processes. Genetic polymorphisms affecting nutrient metabolism could shed light on the inconsistencies among epidemiological studies related to diet and chronic diseases like cancer, diabetes, rheumatoid arthritis, osteoporosis and cardiovascular disease. Genetic variations influence nutrient digestion, absorption, transport, biotransformation, uptake and elimination and can be altered by exposure to bioactive ingredients found in food (El-Sohemy, 2007). These genetic polymorphisms are targets of nutrient action as receptors, enzymes or transporters and can change molecular pathways that influence the physiological response (El-Sohemy, 2007). One functional variant of these genes affects nutrient metabolism by coding for xenobiotic-metabolizing enzymes (drug-metabolizing enzymes). These enzymes are part of phase I and II biotransformation reactions in the liver that produce metabolites resulting in changes of biological activity. Foreign chemicals like antioxidants, vitamins, phytochemicals, caffeine, sterols, fatty acids and alcohol are dietary factors known to alter the expression of these genes.

Much like food derived bioactive compounds, synthetically made products can function in similar pathways with disruptive processes. Organophosphorus (OP) pesticides are one such compound and can cause adverse health effects, especially in children (Lu et al., 2008). These findings from this study suggest that a dietary intake of OP pesticides acts as a major source of exposure in young children (Lu et al., 2008). Organophosphorus (OP) pesticide exposure from diet is not safe for children (Curl, Fenske, & Elgethum, 2003). Organophosphorus pesticide exposure was also studied in farm workers households in agricultural communities (Curl et al., 2002). A chemical called azinphosmethyl was detected in higher concentrations than the other pesticides and the results of this study support a hypothesis that a take-home exposure pathway adds to residential pesticide contamination in agricultural homes; where there are young children present (Curl et al., 2002).

Another study found that the higher incidence of obesity could be due to nutrition, exposure to environmental chemicals or a combination of the two interacting during development (Heindel & vom Saal, 2009). Animal studies show developmental exposure to environmental chemicals increases susceptibility to diseases like obesity. In Brazil for 20 years, dietary risk assessments were done on pesticides, mycotoxins, food additives, heavy metals (like mercury), environmental contaminants (like DDT) and acrylamide, a compound formed during food processing (Caldas & Jardim, 2012). This study showed that cumulative intake of organophosphorus and carbamate pesticides by high consumers of fruits and vegetables is a health concern but the benefits of consuming large amounts of these food groups may overcome those risks (Caldas & Jardim, 2012). 

Genetic polymorphisms as targets of nutrient action offer a solution to issues of exposure by influencing physiological response through dietary interventions (El-Sohemy, 2007). By substituting organic fresh fruits and vegetables for conventional items urinary metabolite concentrations for malathion and chlorpyrifos can be reduced to non detected levels in an organic diet intervention period (Lu et al., 2008). Further, identifying diet-gene interactions can benefit individuals seeking personalized dietary advice and improve public health recommendations by providing sound scientific evidence connecting diet to health (El-Sohemy, 2007). Eliminating exposures to these chemicals and improving nutrition during development also offers the potential for reduction in obesity and other diseases (Heindel & vom Saal, 2009). This would involve limiting the use or eliminating highly toxic pesticides, implementing good agricultural practices to decrease crop contamination, educating local communities about less contaminated foods, and changing dietary habits concerning consumption of high risk, processed food containing toxic chemicals (Caldas & Jardim, 2012).

References

Caldas, E. D., & Jardim, A. N. O. (2012). Exposure to toxic chemicals in the diet: Is the Brazilian population at risk? Journal of Exposure Science & Environmental Epidemiology, 22(1), 1–15. https://doi.org/10.1038/jes.2011.35 or https://pubmed.ncbi.nlm.nih.gov/21989502/

Curl, C. L., Fenske, R. A., Kissel, J. C., Shirai, J. H., Moate, T. F., Griffith, W., . . . Thompson, B. (2002). Evaluation of take-home organophosphorus pesticide exposure among agricultural workers and their children. Environ Health Perspect, 110(12), A787-792. https://pubmed.ncbi.nlm.nih.gov/12460819/

Curl, C. L., Fenske, R. A., & Elgethun, K. (2003). Organophosphorus pesticide exposure of urban and suburban preschool children with organic and conventional diets. Environ Health Perspect, 111(3), 377-382. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1241395/

El-Sohemy, A. (2007). Nutrigenetics. Forum of Nutrition, 60, 25–30. https://doi.org/10.1159/000107064 or https://pubmed.ncbi.nlm.nih.gov/17684398/

Heindel, J. J., & vom Saal, F. S. (2009). Role of nutrition and environmental endocrine disrupting chemicals during the perinatal period on the aetiology of obesity. Molecular and Cellular Endocrinology, 304(1–2), 90–96. https://doi.org/10.1016/j.mce.2009.02.025 or https://pubmed.ncbi.nlm.nih.gov/19433253/

Lu, C., Barr, D. B., Pearson, M. A., & Waller, L. A. (2008). Dietary intake and its contribution to longitudinal organophosphorus pesticide exposure in urban/suburban children. Environ Health Perspect, 116(4), 537-542. doi: 10.1289/ehp.10912 https://pubmed.ncbi.nlm.nih.gov/18414640/