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Background: The SARS-CoV-2 pandemic has highlighted the risk of infection transmission in long-term care facilities (LTCF) and the vulnerability of resident populations. It is essential to understand the environmental spread of the virus and risk of indirect transmission to inform Infection Prevention and Control (IPC) measures in these settings.Methods: Upon notification of SARS-CoV-2 outbreaks, LTCF within a local authority in the South West of England were approached to take part in this pilot study. Investigators visited to swab common touch-points and elevated ‘non-touch’ surfaces and samples were analysed for presence of SARS-CoV-2 genetic material (RNA). Data were collected regarding LTCF infrastructure, staff behaviours, clinical and epidemiological risk factors for infection (staff and residents), and IPC measures.Criteria for success were: recruitment of three LTCF; detection of SARS-COV-2 RNA; variation in proportion of SARS-CoV-2 positive surfaces by sampling zone; potential to assess infection risk from SARS-CoV-2 positive surfaces.Results: Three LTCFs were recruited, ranging in size and resident demographics. Outbreaks lasted 63, 50 and 30 days with resident attack rates of 53%, 40% and 8%, respectively. The proportion of sample sites on which SARS-CoV-2 was detected was highest in rooms occupied by infected residents and varied elsewhere in the LTCF, with low levels in a facility implementing enhanced IPC measures. The heterogeneity of settings and difficulty obtaining data made it difficult to assess association between environmental contamination and infection. Elevated surfaces were more likely to test positive for SARS-CoV-2 RNA than common touch-points.Conclusions: SARS-CoV-2 RNA can be detected in a variety of LTCF outbreak settings. We identified variation in environmental spread which could be associated with implementation of IPC measures, though we were unable to assess the impact on infection risk. Sampling elevated surfaces could add to ongoing public health surveillance for SARS-CoV-2 and other airborne pathogens in LTCF.

INTRODUCTION:\ud \ud Substance use is associated with common mental health disorders, but the causal effect of specific substances is uncertain. We investigate whether adolescent cannabis and cigarette use is associated with incident depression and anxiety, while attempting to account for confounding and reverse causation.\ud METHODS:\ud \ud We used data from ALSPAC, a UK birth cohort study, to investigate associations between cannabis or cigarettes (measured at age 16) and depression or anxiety (measured at age 18), before and after adjustment for pre-birth, childhood and adolescent confounders. Our imputed sample size was 4561 participants.\ud RESULTS:\ud \ud Both cannabis (unadjusted OR 1.50, 95% CI 1.26, 1.80) and cigarette use (OR 1.37, 95% CI 1.16, 1.61) increased the odds of developing depression. Adjustment for pre-birth and childhood confounders partly attenuated these relationships though strong evidence of association persisted for cannabis use. There was weak evidence of association for cannabis (fully adjusted OR 1.30, 95% CI 0.98, 1.72) and insufficient evidence for association for cigarette use (fully adjusted OR = 0.97, 95% CI 0.75, 1.24) after mutually adjusting for each other, or for alcohol or other substance use. Neither cannabis nor cigarette use were associated with anxiety after adjustment for pre-birth and childhood confounders.\ud CONCLUSIONS:\ud \ud Whilst evidence of association between cannabis use and depression persisted after adjusting for pre-term and childhood confounders, our results highlight the difficulties in trying to estimate and interpret independent effects of cannabis and tobacco on psychopathology. Complementary methods are required to robustly examine effects of cannabis and tobacco on psychopathology.