Occupational noise exposure and hypertension: a case-control study

Introduction

Occupational noise exposure in the workplace is a significant health problem in developed and developing countries. In the US, more than 10% of the occupational population are exposed to hazardous noise levels (http://www.cdc.gov/niosh/topics/noise/). In Europe, approximately 20% of workers are exposed to intense noise during at least half of their working time (European Communities 2004). In some developing countries (such as China, India, etc.), this problem may be more serious.

While noise-induced hearing loss (NIHL) is the most investigated and reported health effect related to noise exposure (1-3), other effects such as sleep disturbances (4), digestive disorders (5), changes in the serum cortisol levels (6), higher incidence of occupational accidents and cardiovascular diseases are also considered to be associated with noise exposure (7,8).

Hypertension, which is widely accepted as one of the most common chronic diseases in adults, is a significant risk factor for cardiovascular diseases. It is predicted that 26.4% of the world’s adult population will have hypertension by the year 2025 (9) and approximately 13.5% of the deaths worldwide could be attributed to hypertension (10). The biological possibility of hypertension induced by occupational noise exposure has been described by several studies (8,11-13). However, the association between occupational noise exposure and hypertension continues to be controversial, with several studies showing an association between occupational noise exposure and the risk of persistent hypertension or sustained elevation of blood pressure (14-18), while results from other studies are inconsistent (19-22). The possible reasons for this inconsistency include differences in exposure assessment, study design, numbers of subjects and abilities to control for potential confounding variables.

The aim of this study was to investigate whether occupational noise exposure is associated with a risk of hypertension in a Chinese Han population. A case-control study was conducted which included 286 hypertensive workers and 630 normotensive workers.

Methods

Subjects

The study protocol was approved by the institutional review board of Jiangsu Provincial Center for Disease Prevention and Control. To investigate the association between noise exposure and high blood pressure, we performed an unpaired case-control study including 286 hypertensive workers and 630 normotensive workers between October 2013 and January 2014. All the subjects were Han Chinese. In total, 916 subjects (who had worked a total of 5–30 years) were included and divided into two groups: 454 volunteers identified as noise exposure workers were selected from the Datun Coal and Electricity Company (Xuzhou, China) and 462 volunteers identified as non-noise exposure workers were selected from schools in Datun (Xuzhou, China). The inclusion criteria were as follows: the selected workers were employed for at least 5 years; they had normal blood pressure before being employed (the subjects all had a healthy examination before they were employed); and the selected subjects had not routinely been exposed to other chemical or physical factors associated with hypertension (e.g., vibrations, heat), had no medical factors or diseases that could affect blood pressure, had no family history of hypertension, and had no habit of using hearing protection. The subjects were defined as “ever smokers” if they had smoked 100 cigarettes or more in their lifetimes. The subjects were defined as “ever drinkers” if they had consumed three or more alcoholic drinks per week for at least 1 year (23).

Questionnaire

Structured questionnaires were conducted in face-to-face interviews with each subject. The information collected in the questionnaire included demographic characteristics, lifestyle habits (smoking and alcohol consumption), work history, physical and chemical factor exposure (include noise exposure), disease history, family history of hypertension, informed consent, and other data. All the volunteers were interviewed.

Definition of noise exposure and hypertension

We used sound pressure noise metres (Noise-Pro, Quest, Oconomowoc WI, USA) to detect noise exposure levels at 10 am, 3 pm, 5 pm for three consecutive days at each workplace, according to the China National Criteria for Noise in the Workplace (GBZ43-2002, http://www.zybw.net), and obtained records by normalizing the equivalent continuous A-weighted sound pressure to a nominal 8 h per day (Lex.8 h). Noise exposure levels of teachers of less than 70 dB (A) were defined as non-noise exposure workers [noise exposure levels less than 70 dB (A) do not require noise assessment every year]. Workers of the Datun Coal and Electricity Company with noise exposure levels of more than 80 dB (A), were defined as noise exposure workers [according to the Terms of Occupational Health (GBZ/T 224-2010)].

Blood pressure measurements were taken by the attending physician three times on the left arm with the patient sitting. The blood pressure value used was the mean of these three measurements. The hypertensive workers were defined as having systolic pressure no less than 140 mmHg and/or a diastolic pressure no less than 90 mmHg; subjects with pressures outside these ranges were defined as normotensive workers. Subjects using anti- hypertensive drugs were also classified as hypertensive workers.

Statistical analysis

The data were analysed using SAS statistical software (version 9.1.3; SAS Institute, Cary, NC, USA). Categorical data were analysed using two-sided χ² tests. Continuous data were calculated using independent-sample two-sided t-tests. Unconditional multivariate logistic regressions were applied to compute odds ratios (ORs) and 95% confidence intervals (CIs) to estimate the associations between noise exposure status and risk of hypertension. Adjusted ORs and 95% CIs were calculated by multivariate logistic regression adjusted for age, sex, smoking and drinking status. Furthermore, stratification analyses were performed within different subgroups categorized by noise exposure time, smoking status, and drinking status. All the tests were two-sided and a value of P<0.05 was considered statistically significant.

Results

Characteristics of the study subjects

The demographic and occupational characteristics of the 286 hypertensive workers and 630 normotensive workers are shown in Table 1. Overall, no significant differences were detected in smoking status (P=0.830), drinking status (P=0.443) and noise exposure time (P=0.910). However, we found that hypertensive workers (47.3±7.6 years) were older than normotensive workers (39.3±6.9 years), with P<0.001. When we divided their ages into 3 groups, <35, 35–45, and >45 years, we found that there were more subjects <35 years in the normotensive workers group than in the hypertensive workers group (25.4% vs. 15.0%), but fewer subjects >45 years in the normotensive workers group than in the hypertensive workers group (17.6% vs. 36.7%). The proportion of male workers in the normotensive workers group was less than in the hypertensive workers group (44.0% vs. 69.2%). The effects of smoking and drinking were not analysed quantitatively since the majority of subjects who were smokers and drinkers were light consumers.

Association of noise exposure with the risk of high blood pressure.

As presented in Table 2, among the normotensive workers, the proportions of noise exposure workers and non-noise exposure workers were 46.8% and 53.2%, respectively, and among hypertensive workers, the proportions of noise exposure workers and non-noise exposure workers were 55.6% and 44.4% (P=0.014). When we used the non-noise exposure workers for reference, we found that workers exposed to noise showed an increased risk of hypertension (adjusted OR 1.52, 95% CI: 1.11–2.08).

Stratified analysis of noise exposure associated with hypertension risk

As shown in Table 3, the increased risk effects were more evident in the “ever smoked” group (adjusted OR 2.54, 95% CI: 1.16–5.53). In the “never drink alcohol” group, noise exposure can increase the risk of hypertension, but the risk is lower than the main effect (adjusted OR 1.48, less than 1.52). However, no increased risk was observed in the other groups.

Discussion

In this case-control study, we explored the association between noise exposure and hypertension. We found that subjects with occupational noise exposure had an increased risk of hypertension compared to subjects with non-noise exposure, with the risk being more pronounced in the “ever smoked” group of workers.

In animal studies, spontaneously hypertensive (SH) rats were used to investigate the association between noise exposure and hypertension (24). Borg found that much greater loss of cochlear hair cells in SH rats than in normotensive rats when exposure to high- frequency noise of 100 dB (25). Axelsson et al. also reported that exposure to noise of 100 dB for 10 h induced constriction of precapillary sphincters in radial arterioles and then reduced the blood flow. This phenomenon occurred in both hypertensive and normotensive rats while the effect was more pronounced in the hypertensive group (26). One possible explanation for this difference was vascular damage due to vascular factors such as hypertension. In humans, numerous studies have reported that occupational noise exposure is associated with hypertension (14-17). An exposure-response association between noise-exposure levels and the risk of hypertension was also found in a prospective cohort study (27). This association exist may be due to noise exposure activates the sympathetic and endocrine systems, affecting the humoral and metabolic states of the human organism, leading to the elevation of blood pressure and other biological risk factors (9). Similarly, we found that noise exposure could increase the risk of hypertension in a Chinese population (adjusted OR 1.52, 95% CI: 1.11–2.08).

In general, the cumulative noise exposure (CNE) increases when the noise exposure duration was longer, and the subjects had a higher risk of hypertension (28). Risk can also be influenced by age (29,30) and exposure time (workers exposed to noise longer may be older than workers exposed to noise for a shorter period of time). In our study, we found noise exposure workers in the ≤20 years old exposure group were more susceptible to hypertension (OR 1.55); however, when adjusted for age, sex, smoking and drinking, no increased risk was observed. Similarly, in the >20 years old exposure group, no increased risk was observed. Noise exposure levels are also important risk factors for developing hypertension, and an exposure-response association between noise exposure levels and the risk of hypertension has also been reported (27). However, in our study, noise assessment of non-noise exposure workers was not required, and the data of non-noise exposure workers were missing; therefore, we did not analyse the association between noise exposure and hypertension in the stratification analysis.

Smoking releases norepinephrine through nicotine-induced adrenaline nerve endings leading to the increase of blood pressure. In addition, smoking also causes an acute and marked reduction in radial artery compliance, but this effect being independent of the increase in blood pressure (31). Some studies have also reported that smoking is a risk factor for hypertension. Similarly, in our study, when noise exposure was combined with “ever smoked” status, the increased risk of hypertension was more evident (adjusted OR 2.54, which is higher than 1.52), although the smokers in this study were light consumers (pack-year 8.2). A moderate level of alcohol consumption was associated with an increase in cardiac output and heart rate, leading to increased sympathetic nerve activity (32). Alcohol may also alter the cell membrane by inhibiting intracellular sodium transport, allowing more calcium to enter (33). Alcohol consumption has been shown to be associated with hypertension in many studies (29,34). In this study, we found that in the “never drink” status group, noise exposure could decrease the risk of hypertension (adjusted OR 1.48, which is lower than 1.52).

This study had several limitations that should be considered. First, because it is a cross-sectional study, the direction of association was not clear. Second, some demographic and lifestyle risk factors, such as body mass index (BMI), were not considered. Third, data regarding endogenous variables such as glucose levels, blood cholesterol, cortisol, etc., directly related to coronary heart disease, were omitted from this study. Fourth, the noise exposure levels of non-noise exposure subjects (teachers) were not tested. Finally, the disease outcome used in this investigation was a self-report of the doctor’s diagnosis, which may produce some bias and result in disease misclassification due to inaccurate knowledge or non-reporting.

Conclusions

Our study provided evidence that individuals with occupational noise exposure have an increased risk for hypertension in a Chinese population, this effect was more pronounced in the stratification analysis (in the “ever smoking” group). However, these results need to be validated in a larger population or in a prospective study.

Acknowledgments

Funding: This study was mainly supported by Jiangsu Province’s Outstanding Medical Academic Leader program (LJ201130) and Jiangsu Provincial Youth Medical Talent Program (QNRC2016528).

Footnote

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at http://dx.doi.org/10.21037/jphe.2018.12.01). HS serves as an unpaid Section Editor of Journal of Public Health and Emergency from Jan 2017 to Dec 2019. BZ serves as an Editor-in-Chief of Journal of Public Health and Emergency from January 2017 to December 2022. The other authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. The study was conducted in accordance with the Declaration of Helsinki (as revised in 2013). Human biological samples and animal subjects are not involved in this study, so we don’t need to apply for the ethics approval and patients’ informed consent.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

References

1. Axelsson A, Prasher D. Tinnitus induced by occupational and leisure noise. Noise Health 2000;2:47-54. [PubMed]
2. Dias A, Cordeiro R, Corrente JE, et al. Association between noise-induced hearing loss and tinnitus. Cad Saude Publica 2006;22:63-8. [Crossref] [PubMed]
3. Gomes J, Lloyd O, Norman N. The health of the workers in a rapidly developing country: effects of occupational exposure to noise and heat. Occup Med (Lond) 2002;52:121-28. [Crossref] [PubMed]
4. King RP, Davis JR. Community noise: health effects and management. Int J Hyg Environ Health 2003;206:123-31. [Crossref] [PubMed]
5. Zhang L, Gong JT, Zhang HQ, et al. Melatonin Attenuates Noise Stress-induced Gastrointestinal Motility Disorder and Gastric Stress Ulcer: Role of Gastrointestinal Hormones and Oxidative Stress in Rats. J Neurogastroenterol Motil 2015;21:189-99. [Crossref] [PubMed]
6. Spreng M. Noise induced nocturnal cortisol secretion and tolerable overhead flights. Noise Health 2004;6:35-47. [PubMed]
7. Dias A, Cordeiro R, Goncalves CG. Occupational noise exposure and work accidents. Cad Saude Publica 2006;22:2125-30. [Crossref] [PubMed]
8. Babisch W. Stress hormones in the research on cardiovascular effects of noise. Noise Health 2003;5:1-11. [PubMed]
9. Babisch W. The Noise/Stress Concept, Risk Assessment and Research Needs. Noise Health 2002;4:1-11. [PubMed]
10. Kearney PM, Whelton M, Reynolds K, et al. Global burden of hypertension: analysis of worldwide data. Lancet 2005;365:217-23. [Crossref] [PubMed]
11. Ising H, Kruppa B. Health effects caused by noise: evidence in the literature from the past 25 years. Noise Health 2004;6:5-13. [PubMed]
12. Lozano R, Naghavi M, Foreman K, et al. Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: a systematic analysis for the Global Burden of Disease Study 2010. Lancet 2012;380:2095-128. [Crossref] [PubMed]
13. Lim SS, Vos T, Flaxman AD, et al. A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions, 1990-2010: a systematic analysis for the Global Burden of Disease Study 2010. Lancet 2012;380:2224-60. [Crossref] [PubMed]
14. Sbihi H, Davies HW, Demers PA. Hypertension in noise-exposed sawmill workers: a cohort study. Occup Environ Med 2008;65:643-6. [Crossref] [PubMed]
15. Lee JH, Kang W, Yaang SR, et al. Cohort study for the effect of chronic noise exposure on blood pressure among male workers in Busan, Korea. Am J Ind Med 2009;52:509-17. [Crossref] [PubMed]
16. Chang TY, Jain RM, Wang CS, et al. Effects of occupational noise exposure on blood pressure. J Occup Environ Med 2003;45:1289-96. [Crossref] [PubMed]
17. van Dijk FJ, Souman AM, de Vries FF. Non-auditory effects of noise in industry. VI. A final field study in industry. Int Arch Occup Environ Health 1987;59:133-45. [Crossref] [PubMed]
18. Zhao YM, Zhang SZ, Selvin S. A dose response relation for noise induced hypertension. Br J Ind Med 1991;48:179-84. [PubMed]
19. Aro S. Occupational stress, health-related behavior, and blood pressure: a 5-year follow-up. Prev Med 1984;13:333-48. [Crossref] [PubMed]
20. Hessel PA, Sluis-Cremer GK. Occupational noise exposure and blood pressure: longitudinal and cross-sectional observations in a group of underground miners. Arch Environ Health 1994;49:128-34. [Crossref] [PubMed]
21. Fogari R, Zoppi A, Corradi L. Transient but not sustained blood pressure increments by occupational noise. An ambulatory blood pressure measurement study. J Hypertens 2001;19:1021-7. [Crossref] [PubMed]
22. Inoue M, Laskar MS, Harada N. Cross-sectional study on occupational noise and hypertension in the workplace. Arch Environ Occup Health 2005;60:106-10. [Crossref] [PubMed]
23. Shen H, Huo X, Liu K, et al. Genetic variation in GSTM1 is associated with susceptibility to noise-induced hearing loss in a Chinese population. J Occup Environ Med 2012;54:1157-62. [Crossref] [PubMed]
24. Bianchi G, Fox U, Imbasciati E. The development of a new strain of spontaneously hypertensive rats. Life Sci 1974;14:339-47. [Crossref] [PubMed]
25. Borg E. Noise-induced hearing loss in normotensive and spontaneously hypertensive rats. Hear Res 1982;8:117-30. [Crossref] [PubMed]
26. Axelsson A, Borg E, Hornstrand C. Noise effects on the cochlear vasculature in normotensive and spontaneously hypertensive rats. Acta Otolaryngol 1983;96:215-25. [Crossref] [PubMed]
27. Chang TY, Hwang BF, Liu CS, et al. Occupational noise exposure and incident hypertension in men: a prospective cohort study. Am J Epidemiol 2013;177:818-25. [Crossref] [PubMed]
28. Babisch W, Wolf K, Petz M, et al. Associations between traffic noise, particulate air pollution, hypertension, and isolated systolic hypertension in adults: the KORA study. Environ Health Perspect 2014;122:492-8. [Crossref] [PubMed]
29. Ruixing Y, Shangling P, Shuquan L, et al. Comparison of hypertension and its risk factors between the Guangxi Bai Ku Yao and Han populations. Blood Press 2008;17:306-16. [Crossref] [PubMed]
30. Cohen L, Curhan GC, Forman JP. Influence of age on the association between lifestyle factors and risk of hypertension. J Am Soc Hypertens 2012;6:284-90. [Crossref] [PubMed]
31. Giannattasio C, Mangoni AA, Stella ML, et al. Acute effects of smoking on radial artery compliance in humans. J Hypertens 1994;12:691-6. [Crossref] [PubMed]
32. Grassi GM, Somers VK, Renk WS, et al. Effects of alcohol intake on blood pressure and sympathetic nerve activity in normotensive humans: a preliminary report. J Hypertens Suppl 1989;7:S20-1. [Crossref] [PubMed]
33. Kojima S, Kawano Y, Abe H, et al. Acute effects of alcohol ingestion on blood pressure and erythrocyte sodium concentration. J Hypertens 1993;11:185-90. [Crossref] [PubMed]
34. Shey Wiysonge CU, Ngu Blackett K, Mbuagbaw JN. Risk factors and complications of hypertension in Yaounde, Cameroon. Cardiovasc J S Afr 2004;15:215-9. [PubMed]