Organisms that rely on oxygenic photosynthesis are subject to the effects of photo-oxidative damage, which impairs the function of photosystem-II (PSII). This phenomenon has the potential to lower rates of photosynthesis and diminish plant growth. Experimental evidence shows that the steady-state oxidation-reduction level of the primary quinone acceptor (QA) of PSII is the parameter that controls photodamage under a variety of physiological and environmental conditions. When QA is reduced, excitation energy at PSII is dissipated via a charge-recombination reaction. Such non-assimilatory dissipation of excitation generates singlet oxygen that might act to covalently modify the photochemical reaction center chlorophyll. Under steady-state photosynthesis conditions, the reduction state of QA increases linearly with irradiance, thereby causing a correspondingly linear increase in the probability of photodamage. It is concluded that there is a low probability that photodamage will occur when QA is oxidized and excitation energy is utilized in electron transport, and a significantly higher probability when QA is reduced in the course of steady-state photosynthesis.