Fluoride Action Network



  • Fluoride exposure increased renal injury biomarkers (ALB, Cys-C, KIM-1 and OPN).
  • Fluoride could be considered an environmental kidney toxicant.
  • Exposure to low concentrations of arsenic does not increase kidney injury biomarkers.
  • Co-exposure to low arsenic level does not enhanced renal fluoride toxicity.

Fluoride (F) is a toxicant widely distributed in the environment. Experimental studies have shown kidney toxicity from F exposure. However, co-exposure to arsenic (As) has not been considered, and epidemiological information remains limited. We evaluated the association between F exposure and urinary kidney injury biomarkers and assessed As co-exposure interactions. A cross-sectional study was conducted in 239 adults (18–77 years old) from three communities in Chihuahua, Mexico. Exposure to F was assessed in urine and drinking water, and As in urine samples. We evaluated the urinary concentrations of albumin (ALB), cystatin-C (Cys-C), kidney injury molecule 1 (KIM-1), clusterin (CLU), osteopontin (OPN), and trefoil factor 3 (TFF-3). The estimated glomerular filtration rate (eGFR) was calculated using serum creatinine (Creat) levels. We observed a positive correlation between water and urine F concentrations (?=0.7419, p<0.0001), with median values of 1.5 mg/L and 2µg/mL, respectively, suggesting that drinking water was the main source of F exposure. The geometric mean of urinary As was 18.55 ng/mL, approximately 39% of the urine samples had As concentrations above the human biomonitoring value (15 ng/mL). Multiple linear regression models demonstrated a positive association between urinary F and ALB (ß=0.56, p<0.001), Cys-C (ß=0.022, p=0.001), KIM-1 (ß=0.048, p=0.008), OPN (ß=0.38, p=0.041), and eGFR (ß=0.49, p=0.03); however, CLU (ß=0.07, p=0.100) and TFF-3 (ß=1.14, p=?0.115) did not show significant associations. No interaction with As exposure was observed. In conclusion, F exposure was related to the urinary excretion of early kidney injury biomarkers, supporting the hypothesis of the nephrotoxic role of F exposure.