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A two-hour extension of PT is likely to be more effective in reducing verbal aggression and consumption-related harms than venue lockouts. Modelling a further extension of PT to 24h had minimal additional benefits but the potential to displace incidents of verbal aggression among OU residents from private to public venues.

Taking cues from Science and Technology Studies, we examine how one type of alcohol epidemiology constitutes the causality of alcohol health effects, and how three realities are made along the way: (1) alcohol is a stable agent that acts consistently to produce quantifiable effects;(2) these effects may be amplified or diminished by social or other factors but not mediated in other ways; and (3) alcohol effects observable at the population level are priorities for public health. We describe how these propositions are predicated upon several simplifications and that these simplifications have political implications, including the attribution of responsibility for health effects to a pharmacological substance; the deletion of other agentic forces that might share responsibility; and a prioritization of simple effects over complex effects. We argue that epidemiological research on alcohol might expand its range of ontological, epistemological and methodological practices to identify new ways of understanding and addressing health effects.

It is well established that alcohol-related harm is disproportionately prevalent among low socioeconomic status (SES) drinkers despite their lower consumption of alcohol, but epidemiological investigations have been unable to explain those links causally. I argue that this inability arises from the consumption-as-harm proposition, which proceeds from the assumption that alcohol acts in stable and predictable ways. In this model, ''social factors'' have been associated with increasing or decreasing harms by modulating consumption, but their other transformations of alcohol effects have not been registered.Stepping away from this model, I deploy the notion of the causal assemblage, which was developed in science and technology studies and has recently been applied in studies of alcohol and other drug (AOD) use. I analyze data from interviews with a convenience sample of low SES young adult drinkers and develop case studies of drinking events. I demonstrate that, in the case studies, alcohol-related harms are co-produced by troubled family and ethnic patterns of relations to alcohol and associated memories, enforcement of gender norms in public spaces, and a lack of access to private drinking settings. These insights are significant because they make visible the social forces co-producing alcohol-related harms and demonstrate the limitations of a model of causality commonly deployed in AOD studies.

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