Caspian Journal of

1. Introduction
Cardiovascular Diseases (CVDs) are currently accounted for nearly half of non communicable diseases and are considered as the leading cause of mortality, responsible for 17.3 million deaths per year, a number that is predicted to increase to higher than 23.6 million by 2030 [1, 2]. In 2004, the World Health Organization (WHO) estimated that 12.2% of worldwide deaths were from ischemic heart disease [3]. Rates of mortality from Ischemic Heart Disease (IHD) have declined in most high-income countries, although CVDs still account for one in three deaths in the US in 2008 [4]. In addition, CVDs are the main cause of mortality in the United States, and are considered one of the costliest chronic diseases. As the population ages, CVDs costs are expected to increase substantially [5]. So, it is imperative to identify CVDs’ risk factors and the age groups who are more susceptible to CVDs to be able reduce the rate of CVDs. Many risk factors, which include hypertension, smoking, abdominal obesity, abnormal lipids, and diabetes mellitus, as well as stress and lack of regular physical activity, are significant contributors to cardiovascular mortality, and responsible for more than 90% of all Myocardial Infarctions (MIs) [6, 7]. Some occupational exposures such as noise, air, and radiofrequency transmitters risk factors may result in CVDs [8, 9, 10]. Many workers are consistently under occupational noise exposure, and it has been overlooked in many cases while it is one of the most dangerous risk factors in workplaces.
Occupational noise is a common exposure in the work environment [11]. Surveys show that 23.9% of the working population in Germany are often exposed to noise, and 54% feel burdened by noise [12]. The National Health and Nutrition Examination Survey (NHANES), conducted between 1999 and 2004, found that 17% of workers reported hazardous noise exposure in their workplace in the United States [13]. 
High levels of industrial noise exposure cause a significant risk to health, safety, and hearing acuity [14, 15, 16]. In addition to the association on hearing, nonauditory results such as those on the cardiovascular systems are discussed [11], there is physiological evidence from laboratory and field studies showing that the underlying mechanisms of the cardiovascular associations of noise are unspecified biological stress responses in terms of activation of the autonomic system and neuroendocrine pathways [17, 18]. Noise, as a psychosocial stressor, could lead to dyslipidemia, hypertension, and increased blood glucose, the pathological basis of CVDs [19]. Noise-induced dysregulation may promote the atherosclerotic process, which causes hypertension and cardiovascular events [11].
Although several investigations have shown the association between noise and CVDs, several studies have shown contradictory results [11]. For example, Data from the Copenhagen male study could not determine an association between noise and death from IHD [20], although this paper was excluded because it did not classified different cardiovascular diseases especially myocardial infarction and death and noise levels. In addition, a Finnish enumeration study reported a weak associations [21].In contrast, within the Helsinki heart study, the noise was associated with a moderate but statistically considerable increment in Coronary Heart Disease (CHD) risk that remained even after the workers had passed the age of retirement [22] but this study did not consider lower noise effects so it was excluded. In a Canadian follow-up study investigating lumber mill workers, a Relative Risk (RR) of 1.5 in the highest exposure category was found [23]. Furthermore, although there are some review and meta-analysis articles about the association between noise and CVDs, there is no review and meta-analysis article about the association between occupational noise and CVDs. In the present study, we considered all accessible studies to clarify the association of occupational noise exposure on risk of developing CVDs.

2. Materials and Methods
This study reviewed the published articles investigating the association between occupational noise and MI. Relevant articles were searched from three scientific databases: Scopus, Pubmed, and Web of science. Different combinations of strings using the logical operators’ AND’ and ‘OR’ were used: (“occupational noise” OR “industrial noise” OR “noise exposure”) AND (“MI” OR “coronary heart disease” OR “heart attack” OR “ischemic heart disease” OR “cardiovascular disease” OR “cardiovascular mortality”) without time limitation. Review articles, non-English, non-human studies, conference papers and those articles which did not regard “noise level” or “ noise duration exposure” were excluded.
The remaining articles were screened by two independent researchers based on the following criteria: (1) Relevance of title to the topic of interest (occupational noise and myocardial infraction); (2) Full-text articles published in peer-reviewed journals; and (3) Written in English. A total of eight articles were included in the final review. PRISMA checklist was used for quality assessment. 

3. Results
The initial search identified 517 articles. Titles and abstracts of these articles were screened, and 196 duplicated articles and 207 unrelated articles were excluded. Selected articles were published in English journals. Figure 1 shows the selection process of articles. Eight experimental studies encompassed various aspects of industrial noise.

Included articles were categorized into two main groups; 1) articles that solely assessed the association of occupational noise (level and exposure duration) with CVDs adjusted for a variety (Table 1) , and 2) articles that considered both occupational and environmental or social factors with CVDs (Table 2). 

In Girard et al. study [24], 8910 retired male workers from the Quebec National Institute of Public Health with at least one audiology test in mobile laboratories with no variable adjustment were assessed using a nested case-control study. They defined exposure in term of years of exposure to occupational noise and noise-induced hearing loss. The investigators concluded that Prolonged duration of noise exposure (≥36.5 years) was associated with an increased risk of MI as compared with a shorter period of noise exposure (<27 years). In Eriksson et al. study [25] follow-up data from 7494 people were collected from men living in Gutenburg. Baseline occupation’s data from 1974 to 1977 were considered for classification of occupational noise (Low noise <75 dB(A), Medium noise, 75–85 dB(A), High noise, >85 dB(A) and incidence of CHD and stroke were measured through available data. They revealed that increment in occupational noise increased the risk of CHD, but it does not affect stroke. In Wen Qi et al. study [26], 6307 participants reported exposure to occupational noise and answered health-related questionnaires in a cross-sectional study. In their study, MI prevalence was remarkably higher in people exposed to occupational noise. In Davies et al. [23] cohort study 27,464 workers exposed to occupational noise for more than one year were followed up, and vital status was extracted from the data bank. They reported a strong association between MI and subgroup without hearing protection. In addition, duration of exposure and noise level had significant effects on increasing MI. In Gopinath et al. [27] cross-sectional study 2942 participants reported noise exposure in their workplace by answering a questionnaire about the duration of exposure and mortality from cardiovascular mortality was confirmed by Australian National Death Index.
In Pettersson et al. study [28] Noise exposure w::::as char::::acterized on a job-exposure matrix based on a survey of the working conditions carried out during the mid-1970s. They also assessed the temperature of living region of the participants into reference (Götaland), colder (Svealand), and coldest (Norrland) region and found an interaction between different region and noise exposure on MI but not o stroke. In Selander, 2013 study [29] a population based case-control study conducted on 3050 Participants in Stockholm County and a mixture of residential road traffic noise, job strain and occupational noise were assessed as exposure. MI events was defined as outcome and were checked from hospital discharge registry from 1975 onwards. They found that exposure to traffic and occupational noise simultaneously increased the risk of MI. They reported that mortality from MI and stroke was higher in those with more prolonged exposure to occupational noise. In Kersten et al. [11] study, 4113 people exposed to noise for more than 10 years participated and their jobs were categorized according to ISCO-88. The daily sound exposure was assessed with the help of the machine’s catalogs, and sound levels were into four categories stratified by job complexity according to International Standard Classification of Occupation. They found different association of occupational noise with CVDs in various job demand. 

4. Discussion
Studies showed that occupational noise has some considerable association on increasing risk of CVDs. Other factors, such as environmental conditions and personal and social characteristics, affected risk of CVDs when combined with occupational noise.
Epidemiological studies have shown contradictory associations between noise and CVDs. Copenhagen’s male study data could not detect an association between noise and mortality from IHD [20]. On the other hand, a Canadian follow-up study investigating lumber mill workers found a Relative Risk (RR) of 1.5 within the highest exposure category [23]. The discrepancies derive from differences in noise level, duration of exposure, exposure assessment method, study design, and sample size in various studies [26].
Some studies showed that the duration of exposure to industrial noise has a strong association with MI. In a study from Gopinath, mortality from MI increases when workers are exposed to prolonged periods of occupational noise [27]. in a case-control study conducted by Girard et al., the investigation demonstrated a strong relationship between the duration of exposure to occupational noise and the risk of MI [24]. This result was supported by another study by Qi Gan, where the results show that more prolonged exposure to occupational noise increases the risk of MI [26]. In Davis’s study, results showed an incremented risk of MI in workers without hearing protection, especially in those workers who had longer exposures [23]. 
Six studies have investigated noise level association with and the risk of MI. In a study of acute MI survivors in Berlin [31], subjects self-reported questionnaire shows that high noise levels have a high relative risk with acute MI (3.8), with a positive exposure-response relation. The same conclusion was supported in another study where an association between Moderate and high noise with increasing the risk of MI was observed [32]. Erikson et al. [33] and Virkkunen et al.’s [31] studies were significantly homogenous to be combined in a quantitative meta-analysis. Based on these workers exposed to ≥85 dBA were found to have a 29% higher risk of acquiring IHD, when compared with workers exposed to <85 dBA (RR=1.29, 95% CI 1.15–1.43, 2 studies, about 11,758 participants, I2=0%) [34]. Nonetheless, occupational noise increases the risk of coronary heart diseases; it has been observed that it does not affect heart stroke and MI [25]. A chronic character’s stress-related physiological transformations probably lead to atherosclerosis, hypertension, and ischemic heart disorder [33]. High-level occupational noise may be regarded as a potent external stressor, similar to sudden emotional stress [34] and physical exertion [35], to activate the sympathetic nervous system and endocrine system [36], leading to spasm and subsequent partial or complete coronary occlusion [37, 38, 39]. 
Some factors affect MI combined with noise, such as environmental factors and temperature-related factors. Peterson studied Swedish workers in three main regions exposed to noise and coldness simultaneously; his study showed that the prevalence of MI is higher in colder areas. In a study done by Liu [40], results showed that chronic exposure to environmental risk factors, through sustained changes in the environment, may also predispose to the genesis of CVDs, particularly via potentiation of risk factors such as diabetes and hypertension. In contrast, in the Marchant study, the environmental temperature affects the MI irrespective of the time of the year [41]. In colder situations, Heart rate and blood pressure tend to rise, increasing the myocardial oxygen demand. Hematological variables are also affected, as reflected by increases in thromboglobulin and platelet factor 4, enhancing platelet aggregation [42].
Personal and social factors, such as psychological, physiological, and job characteristics, can affect MI’s prevalence when combined with noise. Selander’s study showed that MI increases in workers exposed to noise and job strain compared to those exposed to noise only [29]. Following this, in a study conducted by Knutsson, MI risk was associated with shiftwork in both genders, men (Odds Ratio [OR]: 1.3, 95% Confidence Interval [95% CI]: 1.1 to 1.6) and women (OR: 1.3, 95% CI: 0.9 to 1.8) [34]. In contrast, in the Marchant study, the environmental temperature affects the MI irrespective of the time of the year [43]. In a study done in Brazil, smoking cigarette per day (OR: 4.90, P<0.00001); glucose waist/hip ratio ≥0.94 (OR: 2.45, P<0.00001); family history of CAD, hypertension (OR: 2.09, P<0.00001) were observed in MI patients [44]. Nine risk factors were associated with MI in women and men. A study performed by Marchant [41] showed that Hypertension, diabetes, moderate alcohol consumption, and physical activity were more extremely associated with MI among women than men. Risk factors associations were normally stronger among the youngsters than older women and men. Many adverse emotions, such as anger, tension, and sadness, resulted in myocardial ischemia [45].
Noise exposure is one of the major risk factors in industries, and in addition, MI is one of the most dominant CVDs among workers. Recognizing risk factors would be essential to reduce the risk of MI. Occupational noise may have some detrimental associations on the heart; therefore, understanding its impact and limitation can be beneficial to deal with this problem. It is suggested that further research would be implemented to assess other environmental factors’ associations on MI.

5. Conclusion
Occupational noise exposure may increase the risk of CVDs, particularly in higher levels and higher duration of exposures. There are also other environmental factors sush as cold temperature, personal and social factors such as job strain, diabetes, smoking, etc., that could interacted with the effect of occupational noise on risk of CVDs. To decrease the risk of CVDs, the noise level and duration of exposure should be minimized to an acceptable level. Furthermore, workers’ health and habits and job demands should be considered by health organization authorities. Although we considered all possible criteria, some deficiencies may be related to the limited number of English studies about the associations of industrial noise on MI and different data collecting methods in the included studies. Additionally, many intervening factors were not considered in many articles.

Ethical Considerations
Compliance with ethical guidelines
This article is a review article with no human or animal sample.

Funding
This research did not receive any grant from funding agencies in the public, commercial, or non-profit sectors.

Authors' contributions
Conceptualization and Supervision: Elahe Oveisi; Methodology: Elahe Oveisi; Investigation, Writing – original draft, and Writing – review & editing: All authors; Data collection: Elahe Oveisi; Data analysis: Elahe Oveisi and Duha Ali. All authors equally contributed to preparing this article.

Conflict of interest
The authors declared no conflict of interest.

Acknowledgments
Thanks to Hamadan University of Medical sciences and Auburn University.

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