The kidneys from 25 patients who received transplants were examined for precise levels of black carbon. The compound forms during high temperature combustion inside car and truck engines using gasoline and diesel fuel. It is emitted from tailpipes where it is breathed in higher amounts by people driving on or living near busy traffic roadways.

Kidney biopsies of transplant patients showed the black carbon particles were being inhaled by the individual and then traveling through the blood and concentrating inside the kidneys over time. Each 10% higher level of black carbon resulted in an 8.24% higher urinary levels of something called KIM-1 and CysC. These two blood markers are used as evidence of kidney damage and building kidney failure. The scientists concluded with the following statement:

"In conclusion, we were able to demonstrate, under real-life exposure conditions, the translocation of inhaled BC (black carbon) particles into the kidneys of kidney transplant recipients. Furthermore, urinary biomarkers, such as KIM-1, a biomarker to assess kidney damage, were linked to higher accumulation of kidney BC load, as well as with ambient BC exposure at the transplant recipients’ residential address and the residential proximity to a major road."
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ABSTRACT:
Background: Ultrafine particles, including black carbon (BC), can reach the systemic circulation and therefore may distribute to distant organs upon inhalation. The kidneys may be particularly vulnerable to the adverse effects of BC exposure due to their filtration function.

Objectives: We hypothesized that BC particles reach the kidneys via the systemic circulation, where the particles may reside in structural components of kidney tissue and impair kidney function.

Methods: In kidney biopsies from 25 transplant patients, we visualized BC particles using white light generation under femtosecond-pulsed illumination. The presence of urinary kidney injury molecule-1 (KIM-1) and cystatin c (CysC) were evaluated with ELISA. We assessed the association between internal and external exposure matrices and urinary biomarkers using Pearson correlation and linear regression models.

Results: BC particles could be identified in all biopsy samples with a geometric mean (5th, 95th percentile) of 1.80 × 103 (3.65 × 102, 7.50 × 103) particles/mm3 kidney tissue, predominantly observed in the interstitium (100 %) and tubules (80 %), followed by the blood vessels and capillaries (40 %), and the glomerulus (24 %). Independent from covariates and potential confounders, we found that each 10 % higher tissue BC load resulted in 8.24 % (p = 0.03) higher urinary KIM-1. In addition, residential proximity to a major road was inversely associated with urinary CysC (+10 % distance: -4.68 %; p = 0.01) and KIM-1 (+10 % distance: -3.99 %; p < 0.01). Other urinary biomarkers, e.g., the estimated glomerular filtration rate or creatinine clearance showed no significant associations.

Discussion and conclusion: Our findings that BC particles accumulate near different structural components of the kidney represent a potential mechanism explaining the detrimental effects of particle air pollution exposure on kidney function. Furthermore, urinary KIM-1 and CysC show potential as air pollution-induced kidney injury biomarkers for taking a first step in addressing the adverse effects BC might exert on kidney function.

Additional statistics on the doubling of kidney disease in all ages since 1990
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8281340/