Int Arch Occup Environ Health DOI 10.1007/s00420-014-0943-8


Cardiovascular disease mortality among retired workers chronically exposed to intense occupational noise Serge Andre Girard • Tony Leroux • Rene´ Verreault • Marile`ne Courteau Michel Picard • Fernand Turcotte • Julie Baril • Olivier Richer

Received: 18 March 2013 / Accepted: 3 April 2014 Ó Springer-Verlag Berlin Heidelberg 2014

Abstract Objective The aim of this study, conducted among retired workers (C65 years), is to estimate the association between long-term risk of cardiovascular disease (CVD) death and (1) duration of occupational noise exposure in career and (2) noise-induced hearing loss (NIHL), the latter being used as an indicator of adverse effects for long-term exposure to occupational noise. Methods Data from screening activities of occupational NIHL were paired to data from death records and were used for this study. A nested case–control analysis was performed. Each case was matched with three controls for length of follow-up and economic sector. A total of 161 CVD deaths occured during an average follow-up of 6.8 years. Conditional logistic regression models were used to estimate the risk (OR) of CVD death by tertiles of duration of noise exposure and of NIHL. Results Conditional logistic regression models indicated that prolonged duration of noise exposure (C36.5 years) (3rd tertile) was associated with an increased risk of CVD

S. A. Girard (&)  M. Courteau  J. Baril  O. Richer Institut national de sante´ publique du Que´bec, Que´bec, Canada e-mail: [email protected]; [email protected] T. Leroux  M. Picard  J. Baril E´cole d’orthophonie et d’audiologie, Universite´ de Montre´al, Montre´al, Canada T. Leroux Laboratoire d’e´tudes sur l’audition, Institut Raymond-Dewar, Centre de recherche interdisciplinaire en re´adaptation, Montre´al, Canada R. Verreault  F. Turcotte De´partement de me´decine sociale et pre´ventive, Universite´ Laval, Que´bec, Canada

death (OR 1.70; 95 % CI 1.10–2.62), as compared with shorter duration (\27 years) (first tertile). Moderate NIHL (2nd tertile) (OR 1.64; 95 % CI 1.04–2.6) and severe NIHL (3rd tertile) (OR 1.66; 95 % CI 1.06–2.60) were also associated with an increase in risk of CVD death. Conclusions Results are consistent with recent findings on the chronic effects of occupational noise exposure persisting after retirement although it is less than during active working life. Keywords Ischemic heart disease  Mortality  Case–control study  Occupational noise exposure  NIHL  Retired workers

Introduction Known to be a stressor stimulating the nervous system, noise is omnipresent both in the environment and in the workplace. WHO estimates that up to 250 million workers around the world are exposed to potentially hazardous noise levels (Concha-Barrientos et al. 2004). In the USA, these estimates vary between 22.4 (Tak et al. 2009) and 30 million (Nelson et al. 2005). The extent of the problem is not well documented in Canada, but up to 400,000 workers are exposed to intense noise in the province of Quebec (Gervais et al. 2006). Noise-induced hearing loss (NIHL) and tinnitus are the most documented effects of noise exposure in the workplace. However, other potentially important health and safety effects, such as increased risk of work-related accidents, falls both during career and in older age, and increased risk of cardiovascular disease (CVD) have been reported (Picard et al. 2008a; Girard et al. 2014; Davies et al. 2005; Gan et al. 2010; Virkkunen et al. 2005, 2006; Heinonen-Guzejev et al. 2007; van


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Kempen et al. 2002; Babisch 2011; Belojevic et al. 2011; Bluhm and Eriksson 2011; Lercher et al. 2011; Maschke 2011; Ndrepepa and Twardelle 2011; Stansfeld and Crombie 2011; Van Kempen 2011). The current state of knowledge identifies two scenarios that establish a relationship between hearing impairment and cardiovascular disease. Independently of occupational or environmental noise exposure, risks factors for systemic cardiovascular diseases such as hypercholesterolemia, atherosclerosis and hypertriglyceridemia and cardiovascular events themselves (angina pectoris, coronary insufficiency, myocardial infarction) have been repeatedly associated with low-frequency hearing loss (0.25–1 kHz in particular) (Gates et al. 1993; Friedland et al. 2009; Fransen et al. 2008; Helzner et al. 2011; Yoshioka et al. 2010; Nash et al. 2011). These new studies specify early works on the influence of cardiovascular health on high- or low-frequency hearing (see Hull and Kerschen 2010 for a review) by stressing the importance of audiometric configuration in the low-frequency spectrum. In this scenario, systemic cardiovascular risk factors and events are thought to disrupt the microarterial blood supply of the stria vascularis at the apex of the cochlea, a region encoding low-frequency sounds (see Hull and Kerschen 2010 again for a contemporary review). There is accumulating evidence suggesting that either CVD itself or its precursors play a role in a form of vascular presbycusis affecting low-frequency hearing as suggested earlier by Johnson and Hawkins (1972) and by Gates et al. (1993). The relationship between low-frequency thresholds and cardiovascular events would in fact be so strong that Friedland et al. (2009) successfully tested a mathematical model that predicts CVD based on low-frequency hearing loss, taking the opposite stand that low-frequency hearing loss is an early biomarker (or diagnostic indicator) of cardiovascular disease—as previously postulated by Susmano and Rosenbush (1988), rather than a consequence of it. In a second scenario, chronic occupational noise exposure would cause not only high-frequency hearing loss (2–6 kHz) but would also act as a stressor leading to cardiovascular diseases (Tomei et al. 2010; Babisch 1998; Davies et al. 2005; Gan et al. 2010). More specifically, prior meta-analyzes on health-related risks of occupational noise exposure reported increased risks for hypertension, opposite to ischemic heart disease and myocardial infarction where results are mitigated (Tomei et al. 2010; Babisch 1998). Noteworthy exceptions are two recent reports by Davies et al. (2005) and Gan et al. (2010), suggesting an increased risk of death from myocardial infarction in a cohort of 50- to 59-year-old workers exposed for C20 years to daily noise levels above 85 dBA. Higher risk of non-fatal coronary heart disease and of isolated diastolic hypertension was also reported among middle-age workers with median duration of occupational exposure of only


8.8 months (Gan et al. 2010). According to major authors in the field, occupational noise exposure is now emerging as an increasingly plausible risk factor for CVD (Virkkunen et al. 2005, 2006; Heinonen-Guzejev et al. 2007; Babisch 2011). Furthermore, the use of NIHL as a biomarker of long-term exposure to occupational noise is emerging as a viable surrogate variable at least to predict the risk for hypertension and the higher occurrence of ECG abnormalities (Chang et al. 2011; Sancini et al. 2012) despite some early dispute on the specificity of NIHL used in this particular respect in lieu of noise exposure levels (see reviews by Topilla et al. 2000, 2001). Although NIHL can be aggravated by some personal conditions such as a genetic tendency to suffer hearing loss and atherosclerosis, or hypertension-induced atherosclerosis (Chang et al. 2011)—thus pressing the need for addressing the issue of reverse causation—one has to realize that these conditions also promote age-related hearing loss (Yoshioka et al. 2010; Topilla et al. 2001). Thus, controlling for age to limit the effect of presbycusis shall help disentangle NIHL from any significant contribution of such pre-existing, nonoccupational confounders, if present. The objective of this case–control study, nested within a cohort of workers screened for possible NIHL, was to examine the association between occupational noise exposure and its resulting permanent hearing loss at frequencies C3 kHz and the long-term risk of CVD death after retirement.

Materials and methods Data sources Two distinct sources of data were used. First, the Quebec National Institute of Public Health (INSPQ, Institut national de sante´ publique du Que´bec) runs a program of hearing testing in the workplace and keeps a computerized database of results from all tests. Methodological details of audiometric tests performed by the INSPQ have been presented in prior publications (Picard et al. 2008a, b). All tests are administered individually using a test protocol based on ISO6189 (1983) standards and works by He´tu et al. (1981) and include provisions related to the reproducibility of audiometric measurements. The INSPQ database was used to identify the study population and to characterize the occupational noise exposure as well as the workers’ hearing status at the time of the hearing test. These data were matched (according to health insurance number, last name, first name and date of birth) with data from the provincial death registry of the Quebec Institute of Statistics (ISQ, Institut de la Statistique du Que´bec), using death records from the Quebec Ministry of Health and Social Services (MSSS, Ministe`re de

Int Arch Occup Environ Health

la sante´ et des services sociaux du Que´bec). This matching provided vital status and cause of death for all subjects in the study cohort. Description of the source population and selection of case–control samples The source population included 8,910 male workers who had at least one audiometric test in mobile laboratories of INSPQ between 1983 and 2005 and who reached the age of 65 (usual retirement age under Canadian social security programs) during the same period. Workers were employed in various industrial sectors and were exposed to noise in their workplace (C80 dBA/8 h) for a large part if not all of their professional life as acknowledged by punctual measurements specific to the work environment at the time of the hearing test. These noise levels are categorized into a dichotomous variable namely in between 80 and 89 dBA or equal to or [90 dBA, which is the daily maximum permissible level of exposure allowed by Quebec regulation for hearing conservation measures to become mandatory (RRQ, S-2.1, r. 13). Among the 8,910 workers of the source population, exactly 50 % (n = 4,455) were in an environment where the noise levels were C90 dBA, while the other 50 % (n = 4,455) were exposed to noise levels \90 dBA. As the study focuses on the impact of occupational noise exposure and as NIHL has its most pronounced effect at 2, 3, 4 and 6 kHz (Dobie 2005), only subjects whose hearing is considered to be normal for age and those whose hearing loss is characteristic of exposure to noise with no other identifiable contributive factor (i.e., workers ‘otologically normal’ in reference to ISO 1999, 1990) are considered for this analysis. To this end, individuals with either one of the following conditions were excluded given the likelihood of non-occupational hearing loss (Picard et al. 2008a, b): 1) history of middle-ear disorders, surgery of the ear or other known ‘personal’ cause of hearing loss (7.8 %); 2) vertigo (4.6 %); 3) abnormal low-frequency tympanometry findings suggesting some other personal hearing condition (42.9 %); 4) asymmetrical hearing loss (between-ear difference in air conduction threshold larger than 20 dB for at least three frequencies or larger than 35 dB for one or two frequencies out of 0.5, 1, 2, 3, 4 and 6 kHz, to expand on Friedland et al. (2009) criterion (13.6 %); 5) median bilateral hearing level at 0.5, 1 and/or 2 kHz exceeding the 90th percentile for age (as per ISO-7029 1999) (31.1 %).This last exclusion criterion was most importantly meant to lessen the odds of pre-existing CVD based on Friedland et al. (2009) findings given that the health status of subjects was unknown at study entry point. To minimize temporal bias in audiometric data and durations of noise exposure, only workers between the age of 55 and 64 at the

time of the hearing test were included in the analyses. Follow-up started on the day of the 65th anniversary of the worker and ended either on the date of death, or on December 31, 2007. Since only month and year of death were available, end of follow-up was determined as the 15th day of the month for deceased subjects. Applying all these criteria to the source population left a potential for 2,943 participants, and 2,581 workers were excluded. Comparisons between the study population and the group of workers with a non-occupational hearing loss show no statistical difference in relation to the duration of exposure and noise levels. However, a more severe mean hearing deficit is observed among workers excluded (42.4 vs. 46.3) (p \ 0.0001). This was expected considering the fact that exclusion criteria are potentially aggravating conditions. Among the 2,943 workers of the cohort who met the criteria for inclusion in this study, 162 (5.5 %) died of CVD during follow-up. With one exception, each CVD death was paired with three controls on the basis of duration of follow-up and industrial sector classification which was then used by the Quebec Workers Compensation Board (BSQ 1990), regardless of the specific sub-sector or occupation. Workers included in the case–control analysis were employed mainly in the following industrial sectors: fabricated metal product manufacturing (21.7 %), transportation equipment manufacturing (10.6 %), mining and quarrying (9.9 %), forestry and sawmills (9.3 %) and wood product manufacturing (8.1 %). Matching was possible for all but one case, and all analyses were therefore based on 644 workers (161 cases and 483 controls). Figure 1 illustrates how participants were selected. Variables Duration of exposure in a noisy workplace was defined as the number of years of exposure to occupational noise, as reported by workers in an individual auditory history questionnaire collected at the time of the hearing test regardless of noisy leisure activities. Average duration of occupational noise exposure of the study population was equivalent to 30.5 years, indicating workers’ long experience in noisy environments. Hearing loss was determined using INSPQ audiometric test results at higher frequencies of 3, 4 and 6 kHz. For a given frequency, hearing was calculated as the bilateral average of hearing level by air conduction. Workers’ hearing loss for all higher frequencies was calculated as the mean losses at individual frequencies. Noise levels in the workplace were assessed by industrial hygienists from the public health network in the weeks preceding audiometric testing sessions. These assessments were used to define noise exposure in the workplace and represent a single measurement specific to the workplace


Int Arch Occup Environ Health Fig. 1 Selection of case– control sample

Population source 8910 male workers with hearing test between 1983 and 2005

Reference population 5524 workers 55 years at last hearing test

Study population 2943 workers otologically normal

Exclusions 3386 workers < 55 at last hearing test

Exclusions 2581 workers with non-occupational hearing loss

162 deaths by CVD

161 deaths by CVD with possible pairing (Cases)

environment at the time of the hearing test. They do not reflect the worker’s career exposure to noise and as such were only considered in descriptive analyses. Noise levels are only available in categories: \90 or C90 dBA. CVD death was ascertained using codes of the International Classification of Diseases: ICD-9 codes 390–459 and ICD-10 codes I00–I99 (OMS 1975, 2008). Use of either classification (ICD-9 or ICD-10) depended on the time when the event occurred. Diagnoses were grouped into the same categories used by Davies et al. (2005): acute myocardial infarction, other ischemic heart disease and other CVD. Data analysis As indicated in Fig. 1, a nested case–control analysis was conducted with each CVD death being matched with three controls on the basis of duration of follow-up (in years) and industrial sector. Follow-up began at age 65. Therefore, age equals to 65? duration of follow-up. Controls could be workers still alive at the end of the study, or workers whose death was not related to heart disease. Duration of follow-up was used as a matching variable in order to control for worker’s age in all comparisons given the correspondence between the two variables (age equals to 65? duration of follow-up). Benefits of this approach are at least twofold. On the one hand, matching on duration of follow-up should limit the deleterious effect of


483 controls Paired on the base of follow –up duration and industrial sector -

aging on CVD (Jousilahti et al. 1999). Furthermore, it should help free high-frequency hearing measurements from any significant contribution of presbycusis and genetic factors mentioned by Chang et al. (2011) as might also be associated with age-related hearing loss (Yoshioka et al. 2010; Topilla et al. 2001). While presbycusis has been shown to compound with NIHL (additive effect according to ISO 1999, 1990), not controlling for this variable might act to obscure NIHL as a biomarker of long-term exposure to occupational noise and thereof causality of CVD death in the present case–control design. Industrial sector was used as a surrogate-matching variable in an effort to take into account socioeconomic variables (such as education and income), general health hazards (such as smoking and alcohol consumption), specific occupational risks (such as workload, shift work, use of vibration tools and ototoxic agents) and environmental exposure (traffic noise), as these co-variables were not available in the original databases. This approach was based on the assumption that co-workers in the same occupational category share many characteristics related to these risk factors. Although an imperfect strategy, it was felt that matching cases and controls in this manner remains a reasonable means to control for these variables and increase comparability of workers. Conditional logistic regression models were used to estimate the relative risk of CVD death first by categories of duration of occupational exposure to noise and by

Hearing treshold levels (dB HL)

Int Arch Occup Environ Health Table 1 Comparison of cases and controls



Cases N = 161

Controls N = 483

p value

Mild loss

Mean age at hearing test (years)




Moderate loss

Mean duration of exposure to noise (years)




Average bilateral hearing loss (dB HL)




Noise level C90 dBA/8 h (%)




10 20 30 40 50 60

Severe loss

70 500






Hz Tertile 1

Tertile 2

Tertile 3

Table 2 Specific causes of death by CVD Fig. 2 Group audiograms as a function of tertiles

severity of NIHL. Duration of exposure to noise was categorized into tertiles according to the distribution in the case–control samples: low (\27.0 years), intermediate (27.0–36.4 years) and high (C36.5 years). Hearing loss was also categorized into tertiles just like in the Gan et al. (2010) study: mild (\33 dB HL), moderate (33–51.4 dB HL) and severe (C51.5 dB HL) (Fig. 2). With duration of follow-up controlling for presbycusis, high-frequency hearing loss was used as a biomarker of adverse effects for long-term exposure to occupational noise in a manner similar to Chang et al. (2011). Verifications for the absence of excessive collinearity between these two predictor variables yielded low estimates of the variance inflation factor (VIF B1.37), clearly below fence of VIF [2.5 suggested by Allison (1999). Note that Spearman rho of 0.155 between the two variables (p \ 0.001) is of the same order of magnitude as the ones reported by Chang et al. (2011) between high-frequency hearing levels and noise levels. Although weak, this correlation suggests that noise levels, duration of exposure and NIHL as a biomarker represent relatively independent, yet relevant and complementary dimensions of adverse auditory effects of occupational noise exposure in career. One reason for the weak correlation may simply be that controlling for age through duration of follow-up plus the restriction imposed on age at the reference audiogram (55–64 years o.) to minimize temporal bias may have contributed to downsize the particular contribution of duration of noise exposure to NIHL, to a more realistic level and possibly, a more truthful measurement. Since cases and controls were matched according to industrial sector and duration of follow-up beginning at 65, these variables were not included in the regression models. Other known risk factors for CVD, such as smoking and previous episodes of CVD, were not available in the source databases and thus could not be added to the models.

Causes of death


Proportion (%)

Acute myocardial infarction (ICD-9: 410)



Other ischemic heart disease (ICD-9: 411–414 ? 429.2)







Other CVD [CI M9 390–405; 415–459 (except 429.2)] Total

Table 3 Univariate conditional logistic regressions Variables



Odds ratio (OR)

95 % CI

Duration of noise exposure


\27 years



27–36.4 years




C36.5 years



Hearing loss

Mild Moderate

\33 dB HL 33–51.4 dB HL

1.00 1.66

– 1.06–2.61


C51.5 dB HL



CI confidence interval

Results Mean age at death for CVD cases was 71.8 years. Average bilateral hearing loss was 44.5 dB HL for cases and 41.2 dB HL for controls (p = 0.03). Noise levels in the workplace at the time of the last hearing test exceeded 90 dBA/8 h in 46.0 and 50.9 % for cases and controls, respectively (p = 0.27). Average duration of exposure in a noisy workplace was 31.9 years for cases, as compared to 29.8 years for controls (p = 0.03) (Table 1). Finally, myocardial infarction was the main cause of CVD death (42.9 %) (Table 2). Table 3 presents the results of conditional logistic regression analyses. The highest tertile of duration of noise exposure in career (C36.5 years) was associated with a


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statistically significant increase in risk of CVD death (OR 1.70; 95 % CI 1.10–2.62), as compared with the first tertile. Similarly, the risk of CVD death increased progressively with the severity of hearing loss, with an OR of 1.66 (95 % CI 1.06–2.61) and 1.64 (95 % CI 1.04–2.60), for the second and third tertiles, respectively, as compared with the first tertile. Separate analyses within categories of CVD death yielded similar results but did not reach statistical significance due to lack of statistical power (results not shown). Further analyses using duration of noise exposure and severity of hearing loss as continuous variables provide similar results (OR 1.02 per year of duration; 95 % CI 1.002–1.05 and OR 1.013 per dB of hearing loss; 95 % CI 1.001–1.03).

Discussion This study showed a statistically significant association between longer duration of occupational noise exposure (C36.5 years) at levels C80 dBA and subsequent risk of CVD death after retirement. Moderate (33–51.4 dB HL) or severe (C51.5 dB HL) permanent hearing loss acquired in the workplace was also associated with an increased risk of CVD death after retirement. These findings are consistent with the recent literature on the long-term cardiovascular risks of occupational noise exposure including the clinical consequence of NIHL in extension of Chang et al. (2011) findings. Virkkunen et al. (2006) observed a statistically significant positive association between the risk of coronary heart disease (CHD) and duration of exposure to noise levels above 80 dBA (RR 1.38 after 9 years and RR 1.54 after 18 years). They also reported an increased CHD risk after age 63 among retired workers exposed to both continuous and impulse noise (RR 1.89; 95 % CI 1.36–2.63). McNamee et al. (2006) observed an increased risk at medium (OR 1.45; 95 % CI 1.02–2.06) and high (OR 1.37; 95 % CI 0.96–1.96) cumulative noise exposure for one of two sites they studied, but judged that their results do not provide clear evidence of an exposure effect between occupational noise exposure and CHD mortality. They explained these results by limitations in the assessment of exposure to noise. The work by Davies et al. (2005) with lumber mill workers revealed an association between a combination of long duration of exposure ([29 years) and high noise level (C95 dBA) with the risk of CVD death. The authors also mentioned that the highest relative risks occurred during subjects’ working years, when they were presumably still exposed to noise. Gan et al. (2010) found similar results for angina pectoris (RR 2.91; 95 % CI 1.35–6.26) and myocardial infarction (RR 2.04; 95 % CI 1.16–3.58) in a population in their early forties exposed for a short period of time. For each category of CVD


examined, duration of noise exposure was incrementally related to risk, irrespective of noise level. As a whole, current findings support the hypothesis of chronic health effects following long-term exposure to occupational noise. Tentative explanations for the association between occupational exposure and risk of CVD mortality include: 1) the noise–stress connection, i.e., stress-related physiological changes of a chronic character presumably leading to atherosclerosis, hypertension and ischemic heart disease (Babisch 2011); and 2) the burden of an anxiety-related stress reaction associated with NIHL, corresponding to a particular case of situational anxiety related to listening difficulties experienced by workers with NIHL both at work and in daily life (Morata et al. 2005; Kochkin and Rogin 2000). Both factors would perpetuate CVD risk even when exposure has permanently ceased (Shalev and Yehuda 1998). The specific role of each of these factors on CVD mortality at retirement age remains to be determined but their contribution to the framework of the general stress theory as described by Babisch (2011) clearly adds to this theoretical rationale. Furthermore, elucidating the particular contribution of noise-induced hearing loss and NIHL-related situational anxiety represents new and innovative avenues of research. Our results suggest that duration of exposure to occupational noise and NIHL act as predictors of CVD death at retirement age, both carrying similar predictive power. Noticeably, susceptible candidates to NIHL would also be more prone to CVD mortality, supporting Chang et al. (2011) and Sancini et al. (2012) findings of a relationship between NIHL and hypertension. The present study has limitations. First, there was some delay between a worker’s last hearing test used to assess exposure and the start of the follow-up, as hearing status was seldom available near the time of retirement. This might have induced some misclassification of the severity of NIHL. Second, despite the nature of the audiometric database, it is impossible to have reliable and accurate information about the different levels of noise to which a worker has been exposed throughout his active professional life. It is therefore not possible to establish a noise exposure dose in career or to assess how noise levels influence the risk of death by CVD. Third, databases did not include information about actual retirement age of workers, which was assumed to be 65 years for all subjects. This might have had some effect as hearing impaired workers would tend to take earlier retirement as mentioned by Christensen (2006), but the real impact of this phenomenon on our results appears small, although it cannot be quantified. Fourth, several potential risk factors for CVD (socioeconomic, general health hazards and specific occupational risk) were not taken into account in the analyses, as they were not available in the source databases. But matching

Int Arch Occup Environ Health

cases and controls for duration of follow-up and industrial sector was made in an effort to minimize this problem and the possible contamination of high-frequency hearing by presbycusis or genetic factors as mentioned by Chang et al. (2011). Fifth, available data do not provide information about a history of heart disease in the study population. Strategy to limit the analysis to hearing loss in high frequencies while controlling for normal for age hearing at 0.5, 1 and/or 2 kHz allowed for a certain form of control to compensate for this. However, this last strategy is only as good as the findings of a strong association between lowfrequency hearing loss and CVD and similarly for those generalizing this relationship to CVD risk factors (Gates et al. 1993; Friedland et al. 2009; Fransen et al. 2008; Helzner et al. 2011). Furthermore, since this study included only retired workers who ended their career in a noisy environment, there might be some under-estimation of the effect of noise on CVD, due to a possible ‘healthy worker effect,’ where workers vulnerable to noise could have left work earlier in the course of their career (Babisch 1998). The magnitude of this phenomenon is, however, difficult to assess. The study was restricted to CVD deaths and did not include non-fatal CVD. This could constitute a source of bias only if the exposure variables (noise exposure and NIHL) are associated with lethality of CVD, in addition to risk.

Conclusion This study supports the hypothesis of an occupational noise—CVD relationship—and stresses the importance of documenting both duration of noise exposure and severity of NIHL, as both factors could act jointly to increase CVD risk. Further studies should investigate mechanisms by which occupational noise and hearing loss may lead to increased risks of cardiovascular diseases. Conflict of interest of interest.

The authors declare that they have no conflict

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Cardiovascular disease mortality among retired workers chronically exposed to intense occupational noise.

The aim of this study, conducted among retired workers (≥65 years), is to estimate the association between long-term risk of cardiovascular disease (C...
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