Noise sensitivity - a stable individual disposition to react negatively to everyday sound - prospectively predicts psychological ill-health, yet it remains unclear whether it marks genuine vulnerability to environmental stressors, is a proxy for chronic anxiety or negative affect, or both, and whether it also signals cardiovascular risk independently of the acoustic exposure level itself. The source study (Stansfeld and Shipley, 2015, Whitehall II cohort) closed with a call for more longitudinal research including measures of noise exposure; its pattern of findings - a mental-health prediction that could not be separated from exposure effects, and an angina association confined to lower employment grades - generated the wider research agenda addressed here: replication in cohorts that measure objective noise exposure alongside noise sensitivity, examination of cardiovascular links in socially disadvantaged populations and of intermediate risk factors (hypertension, inflammatory markers, health behaviours), and psychobiological research on the mechanism connecting noise sensitivity to mental disorder. Later work has partially executed the psychiatric arm: the Caerphilly cohort analysis with modeled road-traffic noise maps confirmed that noise sensitivity predicts psychological ill-health and moderates the noise effect, while the cardiovascular arm remains conflicting and the mechanistic dichotomy unresolved. The open problem is a coherent multi-method empirical objective: establish, in prospectively followed cohorts with objectively assessed noise exposure, whether noise sensitivity predicts incident psychiatric and cardiovascular morbidity and mortality independently of and in interaction with exposure level, through which intermediate risk factors any cardiovascular pathway runs, and which psychobiological account of the trait the evidence supports.

Background

Transportation noise is an established environmental risk factor for cardiovascular disease (CVD), and environmental-noise epidemiology increasingly asks not only how loud the exposure is but who is most harmed by it. Two individual-difference constructs matter here. Noise annoyance is the individually experienced dissatisfaction or disturbance caused by a specific noise source. Noise sensitivity is a broader, relatively stable attitudinal and physiological disposition to be adversely affected by sound in general; it is usually measured with questionnaires such as the Weinstein Noise Sensitivity Scale or brief single items, and it is known to moderate (strengthen) the annoyance response to a given noise level. Objective exposure is quantified by weighted noise metrics such as Lden and Lnight - the average A-weighted sound level over the day-evening-night and night periods at the most exposed facade of a dwelling - obtained from noise maps or measurements rather than self-report.

The question arose from longitudinal analyses of the Whitehall II cohort of British civil servants (Stansfeld and Shipley, 2015), where a single general noise-sensitivity item predicted later depressive symptoms (Center for Epidemiologic Studies Depression Scale) and psychological distress (General Health Questionnaire caseness, OR = 1.56, 95% CI 1.29-1.88) over repeated phases, while showing no association with myocardial infarction, stroke, or mortality except an association with angina in participants from lower employment grades. Because that study measured no objective noise exposure, it could not separate the effect of the disposition from the effect of the noise level itself, nor test their interaction - an interaction that earlier Caerphilly analyses (Stansfeld et al., 1993) had found for psychological morbidity: psychological disorder rose with road-traffic noise level only among the less noise-sensitive men. These findings, together with the paper's closing call for more longitudinal research including measures of noise exposure, shaped the research agenda addressed here.

Several mechanistic hypotheses about what noise sensitivity is have shaped the field. The negative-affect account treats it as a manifestation of a dispositional tendency toward negative self- and situation-evaluation (closely related to chronic anxiety and neuroticism), implying over-reporting of symptoms rather than genuine vulnerability. The general-susceptibility account treats it as one facet of a wider discriminatory capacity for the environment, co-occurring with sensitivity to odours, chemicals, and light. Twin studies estimate the heritability of noise sensitivity - the proportion of trait variation attributable to genetic differences - at roughly 36-40% (Heinonen-Guzejev et al., 2005), which rules out a purely situational state; magneto-/electroencephalography and structural magnetic-resonance imaging show that higher noise sensitivity is associated with altered sound-feature encoding in auditory cortex and with grey-matter volume differences in auditory, limbic (amygdala, hippocampus), and insular regions (Kliuchko et al., 2016; 2018); and secondary analyses found that negative affectivity alone does not explain noise sensitivity (Shepherd et al., 2015). Prospective evidence on incident outcomes with objective exposure - the key to adjudicating between these accounts - has only begun to accumulate (Stansfeld et al., 2021, Caerphilly; SAPALDIA analyses by Eze et al., 2020 and Cerletti et al., 2020), and the cardiovascular branch of the question, including intermediate risk factors such as hypertension, inflammatory markers, and health behaviours and the situation of socially disadvantaged populations, remains open and methodologically demanding.

Problem Statement

Determine, in prospective cohort studies that jointly measure objectively assessed environmental noise exposure (for example, modeled Lden or Lnight at the residence, or measured dosimetry) and noise sensitivity, whether noise sensitivity predicts future illness and mortality independently of noise exposure level, and adjudicate the psychobiological nature of the trait. Concretely: (i) estimate the exposure-adjusted association of noise sensitivity with incident psychiatric outcomes and with incident cardiovascular disease morbidity and mortality, including formal tests of whether noise sensitivity modifies the effect of noise exposure level; (ii) establish whether any cardiovascular association operates through intermediate risk factors - hypertension, inflammatory markers, and health behaviours - and whether it is present in socially disadvantaged populations, where environmental stressor exposure tends to be higher; and (iii) decide between the competing accounts of what noise sensitivity is - a general discriminatory capacity for the environment that co-occurs with sensitivities to other environmental stimuli, a proxy for chronic anxiety or negative affect, or a combination of both - by combining the cohort evidence with psychobiological data (for example, genetically informed, longitudinal, neuroimaging, or auditory-processing designs). Parts (i), (ii) and (iii) are jointly required for a complete determination - answering any one of them resolves that part but leaves the overall problem open. The deliverable is a narrative determination adjudicated from the evidence of existing cohorts and psychobiological studies, not new primary data collection: parts (i) and (ii) are discharged by reporting the exposure-adjusted estimates, interaction tests and mediation evidence already published by the cited cohorts, and part (iii) by weighing the cited cohort and psychobiological findings for and against each account and stating explicitly what the evidence does and does not settle.

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