No. 05 Dr. Stuart Shalat on Tire Particulate Synthetic Turf. February 2017.
No. 04 Impact of tire debris on in vitro and in vivo systems (2005).
No. 03 Inhibition of progesterone receptor activity in recombinant yeast by soot from
fossil fuel combustion emissions and air particulate materials (2005).
No. 02 Genotoxicity of size-fractionated samples of urban particulate matter (2005).
No. 01 Latex Allergens in Tire Dust and Airborne Particles (1996).
The presence of particulate matter (PM) in the environment has been a matter of public health concern for some time now. It is only recently – notably, for example the EHHI study (www.ehhi.org) that the discussion of toxicity and other health effect of artificial turf’s crumb rubber and granulates has called attention to the inhalation and ingestion of crumb rubber that has turned into microscopic dust particles.
Pose a research inquiry for “tire dust” or “TD” with or without “in vitro” and presto (!) up pops a myriad list of articles on studies about the impact of tire dust, as a particulate matter, on lungs and heart, reproductive and genetic material, embryos of different life forms.
In their background, tire dust and crumb rubber have one thing in common, the whole tire. Until someone can show otherwise, the same potential health hazard attributable to tire dust must be presumed to be an aspect of crumb rubber granulates and infill in artificial turf, because the eventual degradation of crumb rubber granulates or infill by human and environmental factors, including climate, produces smaller particles and dust.
It does not take genius to connect the dots here: when the kick of soccer ball spewed the microscopic particulates into the air or when a player inhaled the air right above where her face touched the surface, the tire dust enters rises and enters into the lungs… A mouthpiece that has popped out and reinserted will carry PM with it into an unsuspecting mouth…. What affect any does contact with tire dust have on people who are allergic to latex?
The following synopses may shed some light on the subject or stimulate further research into artificial turf’s contribution to public health problems from a PM perspective.
[No. 05] Dr. Stuart Shalat on Tire Particulate Synthetic Turf. A video presentation accompanying excerpts from a meeting of Consumer Product Safety Commission on 11 January 2017. Presented by Safe Healthy Playing Fields - Coalition www.safehealthyplayingfields.org -- Published by SF Parks on YouTube https://youtu.be/UEVeAmqHTSM (20 January 2017).
|[No. 04] M. Gualtieri, et al., “Impact of tire debris on in vitro and in vivo systems,” in Particle & Fiber Toxicology, vol. 2, no. 1, 2005), published online on March 24, 2005, available on http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1079942.
From the Abstract:
“Background. It is estimated that over 80% of respirable particulate matter (PM10) in cities comes from road transport and that tire and brake wear are responsible for the 3–7% emission of it. Data on the indicators of environmental impact of tire debris (TD), originated from the tire abrasion on roads, are extremely scarce, even though TD contains chemicals (zinc and organic compounds) which can be released in the environment.
“Results. The solution of undiluted 50 g/L TD produced 80.2% mortality (p < 0.01) in X. laevis embryos and this toxic effect was three times greater than that produced by 100 g/L TD. Zn accumulation in HepG2 cells was evident after 4 h exposure. A549 cells exposed to TD organic extract for 72 h presented a modified morphology, a decrease in cell proliferation and an increase in DNA damage as shown by comet assay. The dose 80 μg/ml of TD extract produced 14.6% mortality in X. laevis embryos and 15.9% mortality at 120 μg/ml. Treatment with 80, 100, or 120 μg/ml TD organic extract increased from 14.8% to 37.8% malformed larvae percentages compared to 5.6% in the control.”
“Conclusion. Since the amount of Zn leached from TD is related to pH, aggregation of particles and elution process, the quantity of TD present in the environment has to be taken into account. Moreover the atmospheric conditions, which may deeply influence the particle properties, have to be considered. The TD organic fraction was toxic for cells and organisms. Thus, because of its chemical components, TD may have a potential environmental impact and has to be further investigated.”
From the Conclusion: “Previous work and these results confirm the significant role of zinc in leached TD and the presence of additional organic toxicants. The studies performed have focused their attention on the potential toxic risk to living aquatic organisms from whole rubber tires or scrap. In this study TD has been investigated for its impact on human cell lines and on X. laevis embryos. TD eluates contain zinc, and we have demonstrated that this metal can accumulate in cells, and affect X. laevis embryos. The TD organic extract was toxic to A549 cells and affected cell morphology, cell proliferation and DNA, and produced severe malformations in developing X. laevis embryos. These results contribute to the knowledge of a PM component, which represents a considerable PM10 percentage, which at present is not
considered a 'hazardous substance", but it must be taken into account for its potential environmental impact [footnotes omitted]. Moreover, these results strongly stress the need for further investigation into the distribution of TD as well as on its fate in urban areas.”
[No. 03] J. Wang, et al., “Inhibition of progesterone receptor activity in recombinant
yeast by soot from fossil fuel combustion emissions and air particulate materials,” Science of the Total Environment, vol. 349 (2005), pages 120– 128in (published online on March 11, 2005), available on www.elsevier.com/locate/scitotenv,
The Abstract: “Numerous environmental pollutants have been detected for estrogenic activity by interacting with the estrogen receptor, but little information is available about their interactions with the progesterone receptor. In this study, emission samples generated by fossil fuel combustion (FFC) and air particulate material (APM) collected from an urban location near a traffic line in a big city of China were evaluated to interact with the human progesterone receptor (hPR) signaling pathway by examining their
ability to interact with the activity of hPR expressed in yeast. The results showed that the soot of a petroleum-fired vehicle possessed the most potent anti-progesteronic activity, that of coal-fired stove and diesel fired agrimotor emissions took the second place, and soot samples of coal-fired heating work and electric power station had lesser rogesterone inhibition activity.
The anti-progesteronic activity of APM was between that of soot from petroleum-fired vehicle and soot from coal-fired establishments and diesel fired agrimotor. Since there was no other large pollution source near the APM sampling sites, the endocrine disrupters were most likely from vehicle emissions, tire attrition and house heating sources. The correlation analysis showed that a strong relationship existed between estrogenic activity and anti-progesteronic activity in emissions of fossil fuel combustion. The discoveries that some environmental pollutants with estrogenic activity can also inhibit hPR activity indicate that further studies are required to investigate potential mechanisms for the reported estrogenic activities of these pollutants.” Emphasis added by Synturf.org.
From page 6: “The anti-progesteronic activities in APMs evaluated by IC50 values were lower than that of PFC, but higher than that of the other samples in Table 1. Zhang et al. (2202) [*Note] had evaluated anti-progesteronic activity of tire extracts with IC50 values ranging between 0.07–0.38 mg tire/mL DMSO, very close to that of APM extracts in the present study. Because the IC50 values of APM were close to those of the extracts of PFC, CFS and tires, and the APM sampling sites were close to a traffic line and had no other large pollution source nearby, the presence of anti-progesteronic activity in urban APMs in the present study most likely came from vehicle exhausts, tire attrition and house heating releases. Understanding the effects of FFC and AMP on human and ecological health requires detailed information on their chemical composition.”
[*Note – Synturf.org: Q.H. Zhang, et al., “Antiestrogenic and antiprogesteronic activity of tire extracts with yeast-based steroid hormone receptor gene transcription assay,” in Bulletin of Environmental Contamination Toxicology, December 2002, vol. 69, no. 6, pages 863-868, available on http://www.ncbi.nlm.nih.gov/sites/entrez].
From the Abstract: “Urban particulate matter (UPM) includes particles of size smaller than 10 m (PM10), which may impact on human respiratory and cardiovascular health. It has been reported previously that PM10 can induce DNA damage. We have collected size-fractionated PM10 at the roadside and measured the induction of DNA damage by different-sized UPM… [The] results show that finer particulates have the greatest ability to induce DNA damage in lung epithelial cells and naked DNA, and that both organic and inorganic components of the UPM contribute to its genotoxic effects.
[No. 02 ] K. Healey, et al., “Genotoxicity of size-fractionated samples of urban particulate matter,” in Environmental and Molecular Mutagenesis, vol. 45, issue 4, pages 380-387 (published on line January 20, 2005), available on http://www3.interscience.wiley.com/cgi-bin/abstract/109867012/ABSTRACT?CRETRY=1&SRETRY=0.
[No. 01] A.G. Miguel et al, “Latex Allergens in Tire Dust and Airborne Particles,” in Environmental Health Perspective, vol.104, no. 11, October 1996, available at http://www.ehponline.org/members/1996/104-11/miguel.html.
From the Abstract: “To obtain a wide-spread source for latex exposure, we have considered tire debris. … The inhibition studies with the human IgE latex assay revealed inhibition by the tire tread source samples and ambient freeway dust, as well as by control latex sap and latex glove extracts. …In conclusion, the latex allergens or latex cross-reactive material present in sedimented and airborne particulate material, derived from tire debris, and generated by heavy urban vehicle traffic could be important factors in producing latex allergy and asthma symptoms associated with air pollution particles.”