Tire tread particles turn streams toxic: For coho salmon in the U.S. Pacific Northwest, returning to spawn in urban and suburban streams can be deadly. Regular acute mortality events are tied, in particular, to stormwater runoff, but the identity of the causative toxicant(s) has not been known. Starting from leachate from new and aged tire tread wear particles, Tian et al. followed toxic fractions through chromatography steps, eventually isolating a single molecule that could induce acute toxicity at threshold concentrations of ∼1 microgram per liter. The compound, called 6PPD-quinone, is an oxidation product of an additive intended to prevent damage to tire rubber from ozone. Measurements from road runoff and immediate receiving waters show concentrations of 6PPD-quinone high enough to account for the acute toxicity events. Science , this issue p. 185

This work investigated degradation (measured by qPCR) and biological deactivation (measured by culture-based natural transformation) of extra- and intracellular antibiotic resistance genes (eARGs and iARGs) by free available chlorine (FAC), NH₂Cl, O₃, ClO₂, and UV light (254 nm), and of eARGs by ^•OH, using a chromosomal ARG (blt) of multidrug-resistant Bacillus subtilis 1A189. Rate constants for degradation of four 266–1017 bp amplicons adjacent to or encompassing the acfA mutation enabling blt overexpression increased in proportion to #AT+GC bps/amplicon, or in proportion to #5′-GG-3′ or 5′-TT-3′ doublets/amplicon, with respective values ranging from 0.59 to 2.3 (×10¹¹ M^–1 s^–1) for ^•OH, 1.8–6.9 (×10⁴ M^–1 s^–1) for O₃, 3.9–9.2 (×10³ M^–1 s^–1) for FAC, 0.35–1.2(×10¹ M^–1 s^–1) for ClO₂, and 2.0–8.8 (×10^–2 cm²/mJ) for UV at pH 7, and from 1.7–4.4 M^–1 s^–1 for NH₂Cl at pH 8. For FAC, NH₂Cl, O₃, ClO₂, and UV, ARG deactivation paralleled degradation of amplicons approximating a ∼800–1000 bp acfA-flanking sequence required for natural transformation in B. subtilis, whereas deactivation outpaced degradation for ^•OH. At practical disinfectant exposures, eARGs and iARGs were ≥90% degraded/deactivated by FAC, O₃, and UV, but recalcitrant to NH₂Cl and ClO₂. iARG degradation/deactivation always lagged cell inactivation. These findings provide a quantitative framework for evaluating ARG fate during disinfection/oxidation, and support using qPCR as a proxy for tracking ARG deactivation under carefully selected circumstances.