Tire chemicals found to cause liver damage and brain toxicity

According to new research, a common chemical that accumulates in different organs for tires and their decomposition products has attracted attention to environmental impacts. The study shows that even at concentrations commonly found in urban runoff, these compounds can cause liver damage and behavioral changes in fish over time.

This study, published in environmental science and ecological technology, tracks the impact of 6ppd (a rubber preservative found in almost all tires) and its derivative 6ppd-Quinone (6ppdq) during long-term exposure. Scientists found that the accumulation and damage patterns between the two compounds were very different, and despite the lower liver tissue concentrations, 6PPDQ proved to be more toxic.

What happens when chemicals that protect our tires from wear and tear end up washing streams and rivers? These implications go beyond aquatic ecosystems, as these same compounds are found in various seafood species consumed by humans.

Chemical fingerprints of different organs

The study reveals how these tire-derived chemicals distribute themselves in the body. The parent compound 6ppd preferentially accumulates in the liver and reproductive organs, while its decomposition product 6ppdq is mainly concentrated in the brain, with levels above five times higher than those at 6ppd.

This targeting of different organs helps explain the various toxic effects observed. The brain accumulation of 6ppdq seems particularly relevant to neurological function, and both chemicals ultimately cause liver damage similar to early fatty liver disease.

“This study highlights the hidden threat posed by rubber-derived pollutants in urban runoff,” said Dr. Liangfu Wei, senior author of the study. “Our findings suggest that long-term exposure and its oxidative products can severely disrupt liver metabolism and behavior in aquatic species, even at low levels of 6ppdd. It is worth noting that the toxicity of the transformed product 6ppdq is greater than its predecessor, which is of great significance for regulatory monitoring and pollution control.”

Major findings on chemical toxicity of tires

• 6ppd is mainly accumulated in the liver, while 6ppdq targets the brain
• Both chemicals can lead to growth disorders and changes in swimming behavior
• Exposure causes hepatitis, fat accumulation and cell damage
• Despite lower liver concentrations, 6ppdq proves to be more toxic than its parent compound
• Both compounds destroy lipid and carbohydrate metabolism
• Chemicals inhibit important metabolic regulators (PPARγ) and increase inflammation markers

Exposed signs of liver disease in fish

After three months of exposure to environmentally-related concentrations (2-8 μg/L), zebrafish showed obvious signs of liver damage. Examination of liver tissue showed significant fat accumulation and cellular changes consistent with non-alcoholic fatty liver disease.

Blood tests confirm liver damage, whose enzymes, such as ALT, AST, and ALP, usually indicate liver damage. The researchers also found an increased marker of oxidative stress and inflammation in liver tissue, as well as a depleted antioxidant enzyme that usually protects cells from damage.

Genetic analysis shows that the widespread disruption of metabolic pathways, especially those involved in lipid synthesis, glucose metabolism and cholesterol regulation. The patterns of changes found in early liver disease are very similar to metabolic dysfunction.

Neural effects of behavioral changes

In addition to liver damage, the researchers also observed a large change in behavior in exposed fish. Zebrafish swimming in water containing 6ppd or 6ppdq showed a decrease in swimming distance, an increase in time spent in dark areas of the tank, and a longer fixed period – an indicator of potential anxiety-like behavior and neurological effects.

These behavioral changes appear to depend on dose, while fish exposure to higher concentrations showed a more severe effect. Interestingly, behavioral changes consistent with the reduction in energy production in the liver suggest that chemicals may undermine the body’s ability to produce energy required for normal activities.

The specific accumulation of 6ppdq in brain tissue provides a potential explanation for these behavioral effects, thus raising questions about the possibility that this chemical may affect the nervous system over time.

From fish to humans: potential impact

Although the study focused on zebrafish, it found potential effects on human health. Zebrafish are widely used as model organisms in toxicology because they have many genetic and physiological similarities with humans, especially in metabolic and liver function.

The researchers noted that 6ppd and 6ppdq were found in various aquatic plants consumed by humans, including Snakehead, Weever and Spanish mackerel. Environmental monitoring has found that the concentrations of these compounds are similar to those tested in the global urban runoff water (0.21 to 2.71 μg/L).

Identifying PPARγ as a target for these chemicals is particularly important because the protein plays a crucial role in the regulation of metabolic across vertebrate species. The destruction of PPARγ is related to metabolic diseases and liver disease in humans.

Future research and regulatory considerations

This study highlights the importance of considering parental compounds and their decomposition products when evaluating environmental pollutants. In this case, despite the lower concentration in liver tissue, the transformation product (6ppdq) proved to be more toxic than the original compound.

These findings suggest that current regulatory approaches focusing primarily on parent compounds may underestimate environmental and health risks. The researchers highlight the need for improved urban runoff control and advanced water treatment systems to reduce exposure to these compounds.

Dr. WEI stressed the need for investigation into environmental risk assessments to include parental compounds and their conversion products in regulatory assessments. Given the protection of metabolic pathways across vertebrates, these findings have attracted widespread attention to the potential long-term health effects of tire-derived contaminants on humans through contaminated water sources.

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