Genova Diagnostics toxin testing
Genova offers broad exposure, metal, oxidative-stress and detox-genetics panels. Its strongest mitochondria-adjacent evidence involves heavy metals; no panel can show that a detected chemical caused an individual’s mitochondrial dysfunction.
Lab identity, access and status
Genova Diagnostics, Inc. was founded in 1987 and operates at 63 Zillicoa Street, Asheville, North Carolina, with a Duluth, Georgia site. CLIA 34D0655571; New York PFI #4578; participation in external proficiency programs is reported. Its toxin panels are laboratory-developed tests and, in the sample report’s words, have “not been cleared by the U.S. Food and Drug Administration.” Orders require an authorized provider; Genova Connect uses affiliated physicians. Availability varies, with some offerings unavailable in New York, New Jersey or Rhode Island.
What it sells
Toxic Effects Core
Blood + urine for volatile solvents, chlorinated pesticides, PCBs, organophosphates, BPA, phthalates and parabens. A reseller lists it as “NOT CURRENTLY AVAILABLE”—verify before ordering.
Metals
Toxic Elements–Whole Blood measures aluminum, arsenic, cadmium, lead and mercury. Urine Element Profile accepts post-chelator samples and records “Provoking Status.”
DetoxiGenomic
Buccal SNP panel covering detox-related genes. Common variants generally have small effects, and the panel is not validated to predict mitochondrial outcomes.
Oxidative Stress 2.0
8-OHdG, lipid peroxides and glutathione are oxidative-damage/redox readouts—not direct measurements of mitochondrial function.
Organic-acid panels
Krebs-cycle intermediates feed “mitochondrial dysfunction” functional-imbalance scores. Such metabolites are established in inborn errors of metabolism; wellness extrapolation from mild deviations is not.
Price
No patient-facing list price. Comparable functional-lab toxin panels typically cost about $200–$1,200, cash-pay; confirm the exact test, specimen and fee before ordering.
The mitochondrial connection—graded
Best supported: human observational studies connect lead, cadmium, mercury and arsenic exposure with mitochondrial biomarkers such as mtDNA copy number and 8-OHdG. Directions conflict and causality is unresolved, so an individual blood or urine result cannot establish mitochondrial damage.
Mechanistically plausible: DDE and organophosphate work is largely in vitro or animal at high doses. The pesticides with the strongest human Parkinson’s epidemiology—rotenone and paraquat—are not analytes on Genova’s panels. Oxidative-stress markers are biologically relevant but nonspecific.
Extrapolated: DetoxiGenomic SNPs as predictors of toxin-related mitochondrial outcomes, and mild Krebs-intermediate deviations as a general mitochondrial diagnosis. No validated clinical test of toxin-induced mitochondrial damage exists. Read the toxin foundation guide.
The American College of Medical Toxicology says post-chelator urine metal testing “has not been scientifically validated, has no demonstrated benefit, and may be harmful.” There are no validated reference ranges for provoked urine, and a prospective cohort found these results did not predict heavy-metal poisoning. Genova records provoking status rather than rejecting such samples.
CDC/NIOSH has also documented misuse of unvalidated urine mycotoxin tests: dietary exposure can yield positives in healthy people, and no disease-predictive levels are established. ACMT’s 2025 mold statement says urine mycotoxins should not be attributed to remote inhalation exposure.