Perro and Adams, 2017
Perro, Michelle and Adams, Vincanne, “What’s Making Our Children Sick? How Industrial Food Is Causing an Epidemic of Chronic Illness, and What Parents (and Doctors) Can Do About It,” Chelsea Green Publishing, 2017.
SUMMARY:
With chronic disorders among American children reaching epidemic levels, hundreds of thousands of parents are desperately seeking solutions to their children’s declining health, often with little medical guidance from the experts. What’s Making Our Children Sick? convincingly explains how agrochemical industrial production and genetic modification of foods is a culprit in this epidemic. Is it the only culprit? No. Most chronic health disorders have multiple causes and require careful disentanglement and complex treatments. But what if toxicants in our foods are a major culprit, one that, if corrected, could lead to tangible results and increased health? Using patient accounts of their clinical experiences and new medical insights about pathogenesis of chronic pediatric disorders—taking us into gut dysfunction and the microbiome, as well as the politics of food science—this book connects the dots to explain our kids’ ailing health.
What’s Making Our Children Sick? explores the frightening links between our efforts to create higher-yield, cost-efficient foods and an explosion of childhood morbidity, but it also offers hope and a path to effecting change. The predicament we now face is simple. Agroindustrial “innovation” in a previous era hoped to prevent the ecosystem disaster of DDT predicted in Rachel Carson’s seminal book in 1962, Silent Spring. However, this industrial agriculture movement has created a worse disaster: a toxic environment and, consequently, a toxic food supply. Pesticide use is at an all-time high, despite the fact that biotechnologies aimed to reduce the need for them in the first place. Today these chemicals find their way into our livestock and food crop industries and ultimately onto our plates. Many of these pesticides are the modern day equivalent of DDT. However, scant research exists on the chemical soup of poisons that our children consume on a daily basis. As our food supply environment reels under the pressures of industrialization via agrochemicals, our kids have become the walking evidence of this failed experiment. What’s Making Our Children Sick? exposes our current predicament and offers insight on the medical responses that are available, both to heal our kids and to reverse the compromised health of our food supply.
Zanardi et al., 2020
Zanardi, M. V., Schimpf, M. G., Gastiazoro, M. P., Milesi, M. M., Munoz-de-Toro, M., Varayoud, J., & Durando, M.; “Glyphosate-based herbicide induces hyperplastic ducts in the mammary gland of aging Wistar rats;” Molecular and Cellular Endocrinology, 2019, 501, 110658; DOI: 10.1016/j.mce.2019.110658.
ABSTRACT:
Glyphosate-based herbicide (GBH) exposure is known to have adverse effects on endocrine-related tissues. Here, we aimed to determine whether early postnatal exposure to a GBH induces long-term effects on the rat mammary gland. Thus, female Wistar pups were injected with saline solution (Control) or GBH (2 mg glyphosate/kg/day) on postnatal days (PND) 1, 3, 5 and 7. At 20 months of age, mammary gland samples were collected to determine histomorphological features, proliferation index and the expression of steroid hormone receptors expression, by immunohistochemistry, and serum samples were collected to assess 17beta-estradiol (E2) and progesterone (P4) levels. GBH exposure induced morphological changes evidenced by a higher percentage of hyperplastic ducts and a fibroblastic-like stroma in the mammary gland. GBH-treated rats also showed a high expression of steroid hormone receptors in hyperplastic ducts. The results indicate that early postnatal exposure to GBH induces long-term alterations in the mammary gland morphology of aging female rats. FULL TEXT
McDermott et al., 2019
McDermott, S., Hailer, M. K., & Lead, J. R.; “Meconium identifies high levels of metals in newborns from a mining community in the U.S;” Science of the Total Environment, 2019, 135528; DOI: 10.1016/j.scitotenv.2019.135528.
ABSTRACT:
BACKGROUND: This pilot study was conducted to determine if we could identify intrauterine exposure to metals in meconium, as a measure of exposure for mother-child pairs living in proximity to a mining operation.
OBJECTIVES: We used meconium as a means to measure metal exposure in utero. We set out to quantify the exposure to selected metals that are currently being mined and also are found in the Superfund site in Butte, Montana, and to compare it to that of Columbia, South Carolina, US, where mining is not occurring.
METHODS: This cross-sectional study was conducted between May and November 2018. We received Institutional Review Board approval and we consented women following the birth of their newborns, and collected meconium within 24 h of birth, without any identifiers. Each laboratory used the same protocol for collection, transport, and storage; and the same laboratory protocol was used for the analysis of all samples. Samples were digested using standard acid/peroxide digestion methods and measured by inductively coupled plasma mass spectroscopy.
RESULTS: We collected meconium specimens from 17 infants in Columbia, South Carolina and 15 infants in Butte, Montana. The concentrations found in Columbia were in the low mug kg(-1) range (or less) and were similar to the low levels that have been identified in other studies of meconium. The magnitude of the differences in concentrations found in Butte compared to Columbia was 1792 times higher for Cu, 1650 times higher for Mn, and 1883 times higher for Zn.
CONCLUSION: Using meconium to measure exposure of newborns has implications for risk assessment in a mining-exposed population. This approach was inexpensive and thorough. The magnitude of the differences in the metal levels identified from the two study sites suggests there is an urgent need for further research to learn if there are health consequences to these highly exposed infants. FULL TEXT
Ostrea et al., 2006
Ostrea, E. M., Bielawski, D. M., & Posecion Jr., N C; “Meconium analysis to detect fetal exposure to neurotoxicants;” Archives of Disease in Childhood, 2006, 91(8), 628-629; DOI: 10.1136/adc.2006.097956.
ABSTRACT:
Not Available.
Leite et al., 2019
Leite, S. B., Franco de Diana, D. M., Segovia Abreu, J. A., Avalos, D. S., Denis, M. A., Ovelar, C. C., Samaniego Royg, M. J., Thielmann Arbo, B. A., & Corvalan, R.; “DNA damage induced by exposure to pesticides in children of rural areas in Paraguay;” Indian Journal of Medical Research, 2019, 150(3), 290-296; DOI: 10.4103/ijmr.IJMR_1497_17.
ABSTRACT:
BACKGROUND & OBJECTIVES:
Chronic exposure to pesticides can damage DNA and lead to cancer, diabetes, respiratory diseases and neurodegenerative and neurodevelopment disorders. The objective of this study was to determine the frequency of DNA damage through the comet assay and micronucleus (MN) test in two groups of children, under 10 yr of age living in rural Paraguay and in relation to pesticide exposure.
METHODS:
Two groups of 5 to 10 yr old children were formed; the exposed group (group A, n=43), born and currently living in a community dedicated to family agriculture and surrounded by transgenic soybean crops, and the control group (group B, n=41), born and living in a community dedicated to family agriculture with biological control of pests. For each child, 2000 cells were studied for the MN test and 200 cells for the comet assay.
RESULTS:
The comparison between exposed and control children revealed significant differences in biomarkers studied for the measurement of genetic damage (cell death and DNA damage). The median of MN was higher in the exposed group (6 vs. 1) (P <0.001). Binucleated cells (2.9 vs. 0.5, P <0.001); broken eggs (5.5 vs. 1.0, P <0.001); karyorrhexis (6.7 vs. 0.5, P <0.001); kariolysis (14.0 vs. 1.0, P <0.001); pyknosis (7.4 vs. 1.2, P <0.001) and condensed chromatin (25.5 vs. 7.0, P <0.001) were significantly higher in the exposed group. The values of tail length (59.1 vs 37.2 mum); tail moment (TM) (32.8 vs. 14.4 mum); TM olive (15.5 vs. 6); % DNA tail (45.2 vs. 27.6) and % DNA head (54.8 vs. 72.4), were significantly different between the two groups.
INTERPRETATIONS & CONCLUSIONS:
In children exposed to pesticides, a greater genotoxic and cytotoxic effect was observed compared to non-exposed children. Our findings suggest that monitoring of genetic toxicity in population exposed to pesticides and agrochemicals should be done.
Sherwin et al., 2019
Sherwin, E., Bordenstein, S. R., Quinn, J. L., Dinan, T. G., & Cryan, J. F.; “Microbiota and the social brain;” Science, 2019, 366(6465); DOI: 10.1126/science.aar2016.
ABSTRACT:
Sociability can facilitate mutually beneficial outcomes such as division of labor, cooperative care, and increased immunity, but sociability can also promote negative outcomes, including aggression and coercion. Accumulating evidence suggests that symbiotic microorganisms, specifically the microbiota that reside within the gastrointestinal system, may influence neurodevelopment and programming of social behaviors across diverse animal species. This relationship between host and microbes hints that host-microbiota interactions may have influenced the evolution of social behaviors. Indeed, the gastrointestinal microbiota is used by certain species as a means to facilitate communication among conspecifics. Further understanding of how microbiota influence the brain in nature may be helpful for elucidating the causal mechanisms underlying sociability and for generating new therapeutic strategies for social disorders in humans, such as autism spectrum disorders (ASDs). FULL TEXT
Lajmanovich et al., 2019
Lajmanovich, R. C., Peltzer, P. M., Attademo, A. M., Martinuzzi, C. S., Simoniello, M. F., Colussi, C. L., Cuzziol Boccioni, A. P., & Sigrist, M.; “First evaluation of novel potential synergistic effects of glyphosate and arsenic mixture on Rhinella arenarum (Anura: Bufonidae) tadpoles;” Heliyon, 2019, 5(10), e02601; DOI: 10.1016/j.heliyon.2019.e02601.
ABSTRACT:
The toxicity of glyphosate-based herbicide (GBH) and arsenite (As(III)) as individual toxicants and in mixture (50:50 v/v, GBH-As(III)) was determined in Rhinella arenarum tadpoles during acute (48 h) and chronic assays (22 days). In both types of assays, the levels of enzymatic activity [Acetylcholinesterase (AChE), Carboxylesterase (CbE), and Glutathione S-transferase (GST)] and the levels of thyroid hormones (triiodothyronine; T3 and thyroxine; T4) were examined. Additionally, the mitotic index (MI) of red blood cells (RBCs) and DNA damage index were calculated for the chronic assay. The results showed that the LC50 values at 48 h were 45.95 mg/L for GBH, 37.32 mg/L for As(III), and 30.31 mg/L for GBH-As(III) (with similar NOEC = 10 mg/L and LOEC = 20 mg/L between the three treatments). In the acute assay, Marking’s additive index (S = 2.72) indicated synergistic toxicity for GBH-As(III). In larvae treated with GBH and As(III) at the NOEC-48h (10 mg/L), AChE activity increased by 36.25% and 33.05% respectively, CbE activity increased by 22.25% and 39.05 % respectively, and GST activity increased by 46.75% with the individual treatment with GBH and by 131.65 % with the GBH-As(III) mixture. Larvae exposed to the GBH-As(III) mixture also showed increased levels of T4 (25.67 %). In the chronic assay at NOEC-48h/8 (1.25 mg/L), As(III) and GBH-As(III) inhibited AChE activity (by 39.46 % and 35.65%, respectively), but did not alter CbE activity. In addition, As(III) highly increased (93.7 %) GST activity. GBH-As(III) increased T3 (97.34%) and T4 (540.93%) levels. Finally, GBH-As(III) increased the MI of RBCs and DNA damage. This study demonstrated strong synergistic toxicity of the GBH-As(III) mixture, negatively altering antioxidant systems and thyroid hormone levels, with consequences on RBC proliferation and DNA damage in treated R. arenarum tadpoles. FULL TEXT
Ichikawa et al., 2019
Ichikawa, G., Kuribayashi, R., Ikenaka, Y., Ichise, T., Nakayama, S. M. M., Ishizuka, M., Taira, K., Fujioka, K., Sairenchi, T., Kobashi, G., Bonmatin, J. M., & Yoshihara, S.; “LC-ESI/MS/MS analysis of neonicotinoids in urine of very low birth weight infants at birth;” Plos One, 2019, 14(7), e0219208; DOI: 10.1371/journal.pone.0219208.
ABSTRACT:
OBJECTIVES:
Neonicotinoid insecticides are widely used systemic pesticides with nicotinic acetylcholine receptor agonist activity that are a concern as environmental pollutants. Neonicotinoids in humans and the environment have been widely reported, but few studies have examined their presence in fetuses and newborns. The objective of this study is to determine exposure to neonicotinoids and metabolites in very low birth weight (VLBW) infants.
METHODS:
An analytical method for seven neonicotinoids and one neonicotinoid metabolite, N-desmethylacetamiprid (DMAP), in human urine using LC-ESI/MS/MS was developed. This method was used for analysis of 57 urine samples collected within 48 hours after birth from VLBW infants of gestational age 23-34 weeks (male/female = 36/21, small for gestational age (SGA)/appropriate gestational age (AGA) = 6/51) who were admitted to the neonatal intensive care unit of Dokkyo Hospital from January 2009 to December 2010. Sixty-five samples collected on postnatal day 14 (M/F = 37/22, SGA/AGA = 7/52) were also analyzed.
RESULTS:
DMAP, a metabolite of acetamiprid, was detected in 14 urine samples collected at birth (24.6%, median level 0.048 ppb) and in 7 samples collected on postnatal day 14 (11.9%, median level 0.09 ppb). The urinary DMAP detection rate and level were higher in SGA than in AGA infants (both p<0.05). There were no correlations between the DMAP level and infant physique indexes (length, height, and head circumference SD scores).
CONCLUSION:
These results provide the first evidence worldwide of neonicotinoid exposure in newborn babies in the early phase after birth. The findings suggest a need to examine potential neurodevelopmental toxicity of neonicotinoids and metabolites in human fetuses.
Qiu et al., 2020
Qiu, Shengnan, Fu, Huiyang, Zhou, Ruiying, Yang, Zheng, Bai, Guangdong, & Shi, Baoming; “Toxic effects of glyphosate on intestinal morphology, antioxidant capacity and barrier function in weaned piglets;” Ecotoxicology and Environmental Safety, 2020, 187; DOI: 10.1016/j.ecoenv.2019.109846.
ABSTRACT:
At present, the public is paying more attention to the adverse effects of pesticides on human and animal health and the environment. Glyphosate is a broad-spectrum pesticide that is widely used in agricultural production. In this manuscript, the effects of diets containing glyphosate on intestinal morphology, intestinal immune factors, intestinal antioxidant capacity and the mRNA expression associated with the Nrf2 signaling pathway were investigated in weaned piglets. Twenty-eight healthy female hybrid weaned piglets (Duroc × Landrace × Yorkshire) were randomly selected with an average weight of 12.24 ± 0.61 kg. Weaned piglets were randomly assigned into 4 treatment groups and fed a basal diet supplemented with 0, 10, 20, and 40 mg/kg glyphosate for a 35-day feeding trial. We found that glyphosate had no effect on intestinal morphology. In the duodenum, glyphosate increased the activities of CAT and SOD (linear, P < 0.05) and increased the levels of MDA (linear and quadratic, P < 0.05). In the duodenum, glyphosate remarkably increased the relative mRNA expression levels of Nrf2 (linear and quadratic, P < 0.05) and NQO1 (linear and quadratic, P < 0.05) and reduced the relative mRNA expression levels of GPx1, HO-1 and GCLM (linear and quadratic, P < 0.05). In the jejunum, glyphosate remarkably increased the relative mRNA expression levels of Nrf2 (linear and quadratic, P < 0.05) and decreased the relative mRNA expression levels of GCLM (linear and quadratic, P < 0.05). Glyphosate increased the mRNA expression levels of IL-6 in the duodenum (linear and quadratic, P < 0.05) and the mRNA expression levels of IL-6 in the jejunum (linear, P < 0.05). Glyphosate increased the mRNA expression of NF-κB in the jejunum (linear, P = 0.05). Additionally, the results demonstrated that glyphosate linearly decreased the ZO-1 mRNA expression levels in the jejunum and the mRNA expression of claudin-1 in the duodenum (P < 0.05). In the duodenum, glyphosate increased the protein expression levels of Nrf2 (linear, P = 0.025). Overall, glyphosate exposure may result in oxidative stress in the intestines of piglets, which can be alleviated by enhancing the activities of antioxidant enzymes and self-detoxification. FULL TEXT
Daisley et al., 2018
Daisley, B. A., Trinder, M., McDowell, T. W., Collins, S. L., Sumarah, M. W., & Reid, G.; “Microbiota-Mediated Modulation of Organophosphate Insecticide Toxicity by Species-Dependent Interactions with Lactobacilli in a Drosophila melanogaster Insect Model;” Applied and Environmental Microbiology, 2018, 84(9); DOI: 10.1128/AEM.02820-17.
ABSTRACT:
Despite the benefits to the global food supply and agricultural economies, pesticides are believed to pose a threat to the health of both humans and wildlife. Chlorpyrifos (CP), a commonly used organophosphate insecticide, has poor target specificity and causes acute neurotoxicity in a wide range of species via the suppression of acetylcholinesterase. This effect is exacerbated 10- to 100-fold by chlorpyrifos oxon (CPO), a principal metabolite of CP. Since many animal-associated symbiont microorganisms are known to hydrolyze CP into CPO, we used a Drosophila melanogaster insect model to investigate the hypothesis that indigenous and probiotic bacteria could affect CP metabolism and toxicity. Antibiotic-treated and germfree D. melanogaster insects lived significantly longer than their conventionally reared counterparts when exposed to 10 muM CP. Drosophila melanogaster gut-derived Lactobacillus plantarum, but not Acetobacterindonesiensis, was shown to metabolize CP. Liquid chromatography tandem-mass spectrometry confirmed that the L. plantarum isolate preferentially metabolized CP into CPO when grown in CP-spiked culture medium. Further experiments showed that monoassociating germfree D. melanogaster with the L. plantarum isolate could reestablish a conventional-like sensitivity to CP. Interestingly, supplementation with the human probiotic Lactobacillus rhamnosus GG (a strain that binds but does not metabolize CP) significantly increased the survival of the CP-exposed germfree D. melanogaster This suggests strain-specific differences in CP metabolism may exist among lactobacilli and emphasizes the need for further investigation. In summary, these results suggest that (i) CPO formation by the gut microbiota can have biologically relevant consequences for the host, and (ii) probiotic lactobacilli may be beneficial in reducing in vivo CP toxicity.IMPORTANCE An understudied area of research is how the microbiota (microorganisms living in/on an animal) affects the metabolism and toxic outcomes of environmental pollutants such as pesticides. This study focused specifically on how the microbial biotransformation of chlorpyrifos (CP; a common organophosphate insecticide) affected host exposure and toxicity parameters in a Drosophila melanogaster insect model. Our results demonstrate that the biotransformation of CP by the gut microbiota had biologically relevant and toxic consequences on host health and that certain probiotic lactobacilli may be beneficial in reducing CP toxicity. Since inadvertent pesticide exposure is suspected to negatively impact the health of off-target species, these findings may provide useful information for wildlife conservation and environmental sustainability planning. Furthermore, the results highlight the need to consider microbiota composition differences between beneficial and pest insects in future insecticide designs. More broadly, this study supports the use of beneficial microorganisms to modulate the microbiota-mediated biotransformation of xenobiotics. FULL TEXT