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Summary: Literature suggests that unrestricted and undisturbed sleep is vital for basic human function and performance; however, it is unclear as to what amount of sleep disturbance leads to dysregulation in biomarkers, which may underscore the development of adverse health effects. This systematic review aims to identify the amount of sleep disturbance that contributes to biomarker changes as a potential precursor to the development of adverse health effects. English‐language comparative studies available in PubMed, Cochrane Central, EMBASE, and CINAHL databases from 1 January 1980 to 31 July 2021 were searched. Where possible, random‐effects meta‐analyses were used to examine the effect of sleep disturbances on adverse health effects. The risk of bias of individual studies was assessed using the Cochrane Risk of Bias Tool and the Risk of Bias of Nonrandomised Studies – of Exposures instruments and the certainty of the body of evidence for each outcome was assessed using the Grading of Recommendations Assessment, Development and Evaluation approach. The search identified 92 primary studies reporting on blood pressure, hypertension, heart rate, cardiac arrhythmia, cardiac output, waist circumference, cortisol, adrenaline, noradrenaline, immune system markers, glucose, insulin, cholesterol, and triglyceride levels. Although some meta‐analyses suggested there may be an association between sleep disturbances and certain outcomes, the certainty in the evidence was very low due to concerns with risk of bias, inconsistency across exposures, populations, and imprecision in the estimates of effects. Further research is needed to explore the point at which types, levels and duration of sleep disturbances may begin to increase the risk of developing adverse health outcomes to inform and tailor health interventions. [ABSTRACT FROM AUTHOR]

Background: Exposure to noise can increase biological stress reactions and that could increase the risk of stress-related prenatal effects, including adverse obstetric outcomes; however, the association between exposure to noise and adverse obstetric outcomes has not been extensively explored. The objective of this review was to evaluate the evidence between noise exposures and adverse obstetric outcomes, specifically preeclampsia, gestational diabetes, and gestational hypertension.Materials and Methods: A systematic review of English language, comparative studies available in PubMed, Cochrane Central, EMBASE, and CINAHL databases between January 1, 1980 and December 29, 2021 was performed. Risk of bias for individual studies was assessed using the Risk of Bias Instrument for Nonrandomized Studies of Exposures, and the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) approach was used to assess the certainty of the body of evidence for each outcome.Results: Six studies reporting on preeclampsia, gestational diabetes, and gestational hypertension were identified. Although some studies suggested there may be signals of increased responses to increased noise exposure for preeclampsia and gestational hypertension, the certainty in the evidence of an effect of increased noise on all the outcomes was very low due to concerns with risk of bias, inconsistency across studies, and imprecision in the effect estimates.Conclusions: While the certainty of the evidence for noise exposure and adverse obstetric outcomes was very low, the findings from this review may be useful for directing further research in this area, as there is currently limited evidence available. These findings may also be useful for informing guidelines and policies involving noise exposure situations or environments. [ABSTRACT FROM AUTHOR]

Background: : Exposure to acute noise can cause an increase in biological stress reactions, which provides biological plausibility for a potential association between sustained noise exposure and stress-related health effects. However, the certainty in the evidence for an association between exposures to noise on short- and long-term biomarkers of stress has not been widely explored. The objective of this review was to evaluate the strength of evidence between noise exposure and changes in the biological parameters known to contribute to the development of stress-related adverse cardiovascular responses.Materials and Methods: This systematic review comprises English language comparative studies available in PubMed, Cochrane Central, EMBASE, and CINAHL databases from January 1, 1980 to December 29, 2021. Where possible, random-effects meta-analyses were used to examine the effect of noise exposure from various sources on stress-related cardiovascular biomarkers. The risk of bias of individual studies was assessed using the risk of bias of nonrandomized studies of exposures instrument. The certainty of the body of evidence for each outcome was assessed using the Grading of Recommendations Assessment, Development, and Evaluation approach.Results: : The search identified 133 primary studies reporting on blood pressure, hypertension, heart rate, cardiac arrhythmia, vascular resistance, and cardiac output. Meta-analyses of blood pressure, hypertension, and heart rate suggested there may be signals of increased risk in response to a higher noise threshold or incrementally higher levels of noise. Across all outcomes, the certainty of the evidence was very low due to concerns with the risk of bias, inconsistency across exposure sources, populations, and studies and imprecision in the estimates of effects.Conclusions: : This review identifies that exposure to higher levels of noise may increase the risk of some short- and long-term cardiovascular events; however, the certainty of the evidence was very low. This likely represents the inability to compare across the totality of the evidence for each outcome, underscoring the value of continued research in this area. Findings from this review may be used to inform policies of noise reduction or mitigation interventions. [ABSTRACT FROM AUTHOR]

The evidence from previous studies of serum 25-hydroxyvitamin D (25(OH)D) and ovarian cancer risk is not conclusive. However, the 25(OH)D levels were generally only measured in late adulthood, which may not capture the etiologically relevant exposure periods. We investigated predicted 25(OH)D over the adult lifetime in relation to ovarian cancer risk in a population-based case-control study conducted from 2011 to 2016 in Montreal, Canada (n = 490 cases and 896 controls). Predicted 25(OH)D was computed using previously validated regression models. Unconditional multivariable logistic regression models were used to estimate adjusted odds ratios (aORs) and 95% CIs for average predicted 25(OH)D over the adult lifetime and ovarian cancer risk. In addition, the relative importance of different periods of past 25(OH)D exposure was explored using a weighted cumulative exposure (WCE) model. For each 20-nmol/L increase in average predicted 25(OH)D over the adult lifetime, the aOR (95% CI) was 0.73 (0.55-0.96). In WCE analyses, the inverse association was strongest for exposures 5 to 20 years and 35 to 55 years prior to diagnosis, with aORs (95% CIs) of 0.82 (0.69-0.94) and 0.79 (0.66-1.02), respectively, for each 20-nmol/L increase in predicted 25(OH)D. These results support an inverse association between 25(OH)D levels in adulthood and ovarian cancer risk. This article is part of a Special Collection on Gynecological Cancers. [ABSTRACT FROM AUTHOR]

Background: Exposure to noise can increase biological stress reactions, which may increase adverse health effects, including metabolic disorders; however, the certainty in the association between exposure to noise and metabolic outcomes has not been widely explored. The objective of this review is to evaluate the evidence between noise exposures and metabolic effects. Materials and Methods: A systematic review of English and comparative studies available in PubMed, Cochrane Central, EMBASE, and CINAHL databases between January 1, 1980 and December 29, 2021 was performed. Risk of Bias of Nonrandomized Studies of Exposures was used to assess risk of bias of individual studies and certainty of the body of evidence for each outcome was assessed using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach. Results: Fifty-six primary studies reporting on cortisol, cholesterol levels, waist circumference, glucose levels, and adrenaline and/or noradrenaline were identified. Although meta-analyses suggested that there may be an increase in waist circumference and adrenaline with increased noise exposure, the certainty in the evidence is very low. Overall, the certainty in the evidence of an effect of increased noise on all the outcomes were low to very low due to concerns with risk of bias, inconsistency across exposure sources, populations, and studies, and imprecision in the estimates of effects. Conclusions: The certainty of the evidence of increased noise on metabolic effects was low to very low, which likely reflects the inability to compare across the totality of the evidence for each outcome. The findings from this review may be used to inform policies involving noise reduction and mitigation strategies, and to direct further research in areas that currently have limited evidence available. [ABSTRACT FROM AUTHOR]

The purpose of this study is to elucidate the multiple pathways linking shift work exposure to cardiometabolic risk (CMR) through the intermediates of circadian disruption, sleep disturbances, and stress. A cross-sectional study was conducted at Kingston Health Sciences Center that included female hospital workers, 160 who worked a day-only schedule and 168 who worked rotating days and nights. Participants completed questionnaires, a clinical exam, and wore accelerometers to collect sleep data for 8 days. Participants also collected urine samples at each void during a 24-h collection period, on the day shift for day-only workers and the night shift for rotating shift workers, for cortisol and melatonin measures. We adapted and tested a conceptual model proposed by Knutsson and Boggild for circadian disruption, sleep, and stress mechanistic pathways linking shift work to CMR using structural equation modeling techniques. Status as a rotating shift worker was associated with increased circadian disruption of cortisol and melatonin production compared to day-only workers (P <.001). Increased circadian disruption was associated with an increased CMR (P =.01). Rotating shift work was associated with sleep disturbances (P =.002) and increased job stress (P <.001), but neither was associated with CMR. We conclude that rotating shift work is associated indirectly with increased CMR. This association is mediated by circadian disruption as indicated by attenuated melatonin and cortisol, and flatter cortisol curves. [ABSTRACT FROM AUTHOR]