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Article

Increased Risk of Sensorineural Hearing Loss as a Result of Exposure to Air Pollution

1
Department of Medical Research, Tungs’ Taichung Metroharbor Hospital, Taichung 43503, Taiwan
2
Graduate Institute of Biomedical Sciences, China Medical University, Taichung 40402, Taiwan
3
General Education Center, Jen-Teh Junior College of Medicine, Nursing and Management, Miaoli 35664, Taiwan
4
Department of Otolaryngology, Tungs’ Taichung Metroharbor Hospital, Taichung 43503, Taiwan
5
College of Medicine, The School of Chinese Medicine for Post Baccalaureate, I-Shou University (Yancho Campus), Kaohsiung 84001, Taiwan
6
Department of Chinese Medicine, E-DA Hospital, Kaohsiung 82445, Taiwan
7
Department of Chinese Medicine, E-DA Cancer Hospital, Kaohsiung 82445, Taiwan
8
Center for Molecular Medicine, China Medical University Hospital, Taichung 40402, Taiwan
9
Department of Biotechnology, Asia University, Taichung 41354, Taiwan
10
Department of Pediatrics, Department of Medical Research, Tungs’ Taichung Metroharbor Hospital, Taichung 43503, Taiwan
11
Department of Rehabilitation, Jen-Teh Junior College of Medicine, Nursing and Management, Miaoli 35664, Taiwan
12
Department of Thoracic Surgery, Chung Shan Medical University Hospital, Taichung 40201, Taiwan
13
Management Office for Health Data, China Medical University Hospital, Taichung 40402, Taiwan
14
Institute of Biomedical Sciences, Mackay Medical College, New Taipei City 252, Taiwan
*
Author to whom correspondence should be addressed.
First authors.
Int. J. Environ. Res. Public Health 2020, 17(6), 1969; https://0-doi-org.brum.beds.ac.uk/10.3390/ijerph17061969
Received: 23 January 2020 / Revised: 3 March 2020 / Accepted: 11 March 2020 / Published: 17 March 2020
(This article belongs to the Special Issue Environmental Exposures and Hearing Loss)

Abstract

Whether exposure to air pollution is associated with developing sensorineural hearing loss (SHL) remains controversial. Using data from the National Health Insurance Research Database, we recruited a total of 75,767 subjects aged older than 20 years with no history of SHL from 1998 to 2010, and they were followed up until SHL was observed, they withdrew from the National Health Insurance program, or the study ended. The subjects were evenly exposed to low-level, mid-level, and high-level carbon monoxide (CO) and nitrogen dioxide (NO2). The incidence rate ratio of SHL for patients exposed to high-level CO was 1.24 (95% confidence interval (CI) = 1.14–1.36). The NO2 pollutants increased the incidence rate ratios of SHL in mid-level NO2 and high-level NO2 exposures by 1.10 (95% CI = 1.10–1.32) and 1.36 (95% CI = 1.24–1.49) times, respectively. The adjusted hazard ratio (adj. HR) of SHL in patients exposed to high-level CO was 1.45 (95% CI = 1.31–1.59), relative to that of patients exposed to low-level CO. Compared to patients exposed to low-level NO2, patients exposed to mid-level NO2 (adj. HR = 1.40, 95% CI = 1.27–1.54) and high-level NO2 (adj. HR = 1.63, 95% CI = 1.48–1.81) had a higher risk of developing SHL. The increased risk of SHL following the increased concentrations of air pollutants (CO and NO2) was statistically significant in this study. In conclusion, the subjects’ exposure to air pollution exhibited a significantly higher risk of developing SHL in Taiwan.
Keywords: air pollution; sensorineural hearing loss; National Health Insurance Research Database (NHIRD); hazard ratio air pollution; sensorineural hearing loss; National Health Insurance Research Database (NHIRD); hazard ratio

1. Introduction

In developing and developed countries, air pollution has already become an important health issue. Several factors, such as urbanization, industrialization, heavy traffic, or establishment of thermal power stations, result in air pollution in several countries. Primarily, lung cancer is considered the major severe disease caused by air pollution [1,2]. Notably, accumulating evidence shows that chronic exposure to air pollution is associated with not only respiratory diseases but also non-lung cancers [3,4] and cardiovascular [5,6], inflammatory [7,8], and neurodegenerative diseases [9,10] including age-related macular degeneration (AMD) [11].
Sensorineural hearing loss (SHL) is defined as the damage, degeneration, or loss of the cochlear hair cells (HCs) [12,13] or spiral ganglion neurons [14,15,16] in the auditory system. The majority of SHL patients are diagnosed with congenital SHL including syndromic and non-syndromic SHL. It has been shown that a total of 70–100 genetic loci are associated with SHL. These genetic loci are usually found in genes responsible for signal transduction, membrane ion channel expression, HC development, and aging processes [13]. Most of the genes are directly related to the function of the outer HCs in fine-tuning incoming sound waves. Currently, hearing aids and cochlear implants are clinically beneficial in restoring the hearing function of patients with congenital SHL. However, Food and Drug Administration-approved drugs used to treat congenital or degenerative SHL are not yet available.
Several etiological factors can cause SHL, such as loud noise [17,18], viral infection [14,19], genetic mutations [20,21], accidental events [22,23], ototoxicity [24,25,26], autoimmune diseases [27] and unknown illness-induced sudden SHL [28,29]. Several diseases such as hypertension (HT) [30,31], diabetes mellitus (DM) [32,33], stroke [34], chronic kidney disease (CKD) [35,36], ischemic heart disease (IHD) [37,38], alcoholism [39,40], nicotine dependence [41,42], asthma [43,44,45], chronic obstructive pulmonary disease (COPD) [46], and rheumatoid arthritis (RA) [47] are associated with SHL. Notably, some of these diseases can cause defects in the vascular system and microcirculation in the cochlea, subsequently resulting in hypoxia [48,49,50]. Hypoxia has been demonstrated to damage the HCs and neurons in the inner ear [48,50]. Furthermore, it has been shown that hypoxia-inducible factor-1α is upregulated by cobalt chloride-induced hypoxia in noise-induced hearing loss [51].
Accumulating evidence using the analyses of the National Health Insurance Research Database (NHIRD) in Taiwan shows that chronic exposure to air pollution increases the risk of neurodegenerative diseases including Parkinson’s disease (PD) [9], dementia [10], and AMD [11]. Although air pollution has been considered a risk factor for several diseases, its association with hearing disorders has been less studied. A previous study conducted in Busan, Korea, showed that air pollution is possibly associated with sudden SHL [52]. However, whether air pollution is associated with SHL remains controversial. Therefore, it is significantly interesting to hypothesize that air pollution may also be associated with SHL development. In this study, we focused on investigating the two major traffic-related air pollutants: nitrogen dioxide (NO2) and carbon monoxide (CO). We analyzed the data from a longitudinal cohort study using the Taiwan National Health Insurance (NHI) data to assess the significant effects of these traffic-related air pollutants to SHL.

2. Subjects and Methods

2.1. Data Source and Study Subjects

A single-payer Taiwan NHI program was launched in March 1995. Approximately 99% of Taiwan’s population are included in this program. The NHIRD consists of insured’s inpatients and outpatient claims, medications, and treatment data. In the present study, we utilized the Longitudinal Health Insurance Database which is the health database of a million beneficiaries randomly selected from the NHIRD. The identification information was encrypted to protect the patients’ personal privacy. The disease codes were identified according to the International Classification of Disease, Ninth Revision, Clinical Modification (ICD-9-CM). We recruited subjects aged older than 20 years with no history of SHL from 1998 to 2010, and they were followed up until SHL was observed, they withdrew from the NHI program, and the study ended (December 2011).

2.2. Exposure Measurement

The data regarding the air pollutants were collected from 74 ambient air quality monitoring stations across Taiwan. The air quality data are managed by Taiwan Environmental Protection Administration. The annual concentrations of NO2 and CO from 1998 to 2010 were grouped into the following three levels according to tertiles: the low-, mid-, and high-level groups. The NO2 concentrations of the low-, mid-, and high-level groups were <19.53 (ppb), 19.53–25.66 (ppb), and >25.66 (ppb), respectively. Moreover, the CO concentrations of the low-, mid-, and high-level groups were <0.61 (ppm), 0.61–0.76 (ppm), and >0.76 (ppm), respectively. To analyze the exposures across a 13 year period (from 1998 to 2010), we calculated the annual average of pollutants from baseline to the date of hearing loss occurrence.

2.3. Main Outcome and Covariates

Hearing loss (ICD-9-CM code 389.10–389.12 and 388.01) was the primary event in this study. Besides age and sex, we also considered the insurance fee and area of residence of the subjects. The common comorbidities including HT (ICD-9-CM codes 401–405) [30,31], DM (ICD-9-CM code 250) [32,33], stroke (ICD-9-CM codes 430–438) [34], head injury (ICD-9-CM codes 850–854) [22,23], CKD (ICD-9-CM code 585) [35,36], IHD (ICD-9-CM codes 410–414) [37,38], alcoholism (ICD-9-CM codes 305.0 and 303) [39,40], nicotine dependence (ICD-9-CM code 305.1) [41,42], asthma (ICD-9-CM code 493) [43,44,45], COPD (ICD-9-CM codes 490–492, 494, and 496) [46], and RA (ICD-9-CM code 714) [47] were considered as potential confounders.

2.4. Statistical Analysis

We show the demographic distribution as a percentage. The incidence density rates of hearing loss were calculated, and the incidence rate ratio (IRR) was assessed by Poisson regression. We estimated the hazard ratios using the multivariate Cox proportional hazard model, adjusting for age, sex, insurance fee, urbanization, and comorbidities.

3. Results

We recruited 75,767 subjects in the present study. Table 1 shows the distribution of the demographic characteristics of the study sample. The subjects’ mean age was 54.1 (±11.1) years with a mean age of 11.1 (±2.2) years the following years. Moreover, 45.3% of the subjects were men. The subjects were evenly exposed to low-, mid-, and high-level CO and NO2. Most of the subjects lived in moderately urbanized areas (33.1%) and highly urbanized areas (32.5%). Table 2 shows that the top three comorbidities with high incidence rates were HT (57.5%), DM (20.6%), stroke (9.1%), head injury (9.8%), CKD (5.3%), IHD (34.6%), alcoholism (1.4%), nicotine dependence (2.2%), asthma (17.5%), COPD (34.5%), and RA (0.5%).
The IRRs of SHL in different air pollutant exposure levels are presented in Table 3. Subjects exposed to low-level air pollutants were assigned to the reference group. The IRR of SHL in subjects exposed to high-level CO was 1.24 (95% confidence interval (CI) = 1.14–1.36). The NO2 pollutants increased the incidence of SHL in subjects exposed to mid-level NO2 and high-level NO2 by 1.10 (95% CI = 1.10–1.32) and 1.36 (95% CI = 1.24–1.49) times, respectively. From our analyses, the CO levels in highly urbanized region, moderately urbanized region, boomtown, and others were 0.82 ± 0.31, 0.69 ± 0.24, 0.71 ± 0.22, and 0.58 ± 0.21, respectively (Table 3). Furthermore, the NO2 levels in highly urbanized region, moderately urbanized region, boomtown, and others were 24.69 ± 6.65, 21.83 ± 6.45, 23.54 ± 5.53, 17.87 ± 6.37, respectively (Table 3). Our results suggest that the distribution of CO and NO2 levels are highly correlated with the urbanization.
According to Table 4, the adjusted hazard ratio (adj. HR) of SHL in subjects exposed to high-level CO was 1.45 (95% CI = 1.31–1.59), relative to that of subjects exposed to low-level CO. Compared to subjects exposed to low-level NO2, subjects exposed to mid-level NO2 (adj. HR = 1.40, 95% CI = 1.27–1.54) and high-level NO2 (adj. HR = 1.63, 95% CI = 1.48–1.81) had a higher risk of developing SHL. Moreover, the increased risk of SHL following the increased concentrations of air pollutants (CO and NO2) was statistically significant in this study. In the present study, we found that the incidence rate ratio of SHL in the highest level of CO (IRR = 1.24, 95%CI = 1.14–1.36) was significantly higher than that in low level of CO (Table 4). Furthermore, we found that the incidence rate ratio of SHL in the mid-level (IRR = 1.21, 95% CI = 1.10–1.32) and highest level of NO2 (IRR = 1.36, 95% CI = 1.24–1.49) was significantly higher than that in low level of NO2 (Table 4).
According to Table 5, the aHR of hearing loss in the high CO concentration group relative to the low CO concentration group was 1.45 (95% CI, 1.31–1.59). Patients in the mid-NO2 level (aHR = 1.40, 95% CI = 1.27–1.54) and high NO2 level (aHR = 1.63, 95% CI = 1.48–1.81) groups had a higher risk of hearing loss compared to patients in the low NO2 level group. The increased concentrations of the air pollutants (i.e., CO and NO2) enhancing the risk of hearing loss was statistically significant. Moreover, continuous analyses based on the subjects’ sex and age (subjects aged 50 years) to assess the association between air pollution and SHL were performed. Our data suggest that both male (aHR = 1.25, 95% CI = 1.03–1.52) and female (aHR = 1.49, 95% CI = 1.20–1.85) subjects have a significantly high incidence of SHL when they are exposed to CO pollution. Moreover, female subjects had a significantly high incidence of SHL when exposed to NO2 (aHR = 1.01, 95% CI = 1.001–1.02). Furthermore, elderly subjects aged greater than 50 years had a significantly higher risk of SHL (CO: aHR = 1.37, 95% CI = 1.17–1.62) when they were exposed to CO pollution. Additionally, we provided the probability-free prediction of SHL among the three levels of CO and NO2 concentrations (Figure 1).

4. Discussion

Although air pollution has been considered a risk factor for several diseases, its association with hearing disorders has been less studied. In this study, we hypothesized that air pollution may also be associated with SHL development. We focused on investigating the two major traffic-related air pollutants: nitrogen dioxide (NO2) and carbon monoxide (CO). We analyzed the data from a longitudinal cohort study using Taiwan National Health Insurance (NHI) data to assess the significant effects of these traffic-related air pollutants to SHL. Our results revealed that the subjects who were chronically exposed to air pollution were at a significantly increased risk of developing SHL. Based on the longitudinal human data, our results suggest that NO2 and CO could have potential adverse effects on SHL. Furthermore, we showed that long-term exposure to the highest quartile of NO2 significantly increased the risk of SHL by almost 1.63 fold, even after adjusting the confounding factors. Additionally, exposure to the highest quartile of CO also increased the risk of SHL by 1.45 fold. Nitrogen dioxide and CO result in cellular damages through different mechanisms. Nitrogen dioxide is a reactive nitrogen species (RNS). Reactive nitrogen species and reactive oxygen species cause cell apoptosis. On the contrary, CO is considered toxic, as it prevents the blood system from effectively carrying oxygen around the body, specifically to the vital organs such as the heart and brain. However, any report showing the association between CO and SHL does not exist yet. The present study suggests that exposure to CO and NO2 has several adverse effects on the auditory system.
Several studies investigating the clinical effects of air pollution on different organ systems in the human body have been conducted [4,7,8,9,11,53]. Using similar datasets, we have previously shown that CO and NO2 were associated with AMD [11], dementia [53], and PD [9]. Compared with the lowest exposure group, the adj. HRs for AMD and dementia were 1.91 and 1.5 and 1.84 and 1.61 for the highest quartile of NO2 exposure and the highest quartile of CO exposure, respectively. Based on the adj. HRs, our data indicated that these two pollutants have similar adverse effects on SHL, AMD, and dementia. On the contrary, either NO2 or CO is not associated with the incidence of PD. However, particulate matter 10 (PM10) exposure can have significant adverse effects on PD development. Similar to AMD and dementia, SHL is also an age-related disease that primarily affects the cochlear hair cells and spiral ganglion neurons.
The onset of SHL has been associated with several risk factors including inflammation and oxidative stress. Our data further suggest that RNS might also contribute to SHL progression. Nitrogen dioxide is one of the most important components of traffic-related air pollution. It can be hydrolyzed to nitrous and nitric acid, both of which can induce inflammation by oxidative stress and lipid peroxidation. It has been suggested that gentamicin application intratympanally can result in a hearing threshold shift beginning on the second day after gentamicin application. This hearing impairment is simultaneously associated with an increased NO2 (a stable oxidation product of NO2) concentration in the lateral wall, indicating that NO2 contributes to gentamicin-induced hearing impairment [54].
Although the primary route of exposure to NO2 is via inhalation, studies assessed not only the association between the respiratory system and NO2 exposure but also the association between the cardiovascular [55,56] and neurological systems and NO2 exposure [57]. Previously, air pollution has been reported to be a risk factor for sudden SHL [52]. The major differences between our results and the reports of Lee et al. [52] are as follows: (1) our study was the first study to use a large longitudinal cohort from 1998 to 2010 to demonstrate the significant association between SHL and high levels of ambient NO2 and CO. (2) According to the report of Lee et al. [52], they utilized the data from the daily patient numbers admitted to the hospital with sudden SHL in 2015 and demonstrated that in Busan, Korea, there is a statistically significant weak association between the daily numbers of patients admitted to the hospital with sudden SHL and the exposure of mean daily PM10 and PM2.5 concentrations [52].
It has been suggested that the risk of SHL is also significantly associated with factory workers who are co-exposed to noise and heavy metals or organic solvents [58]. Co-exposure to noise and heavy metal or toxic pollution results in a worse SHL compared with isolated exposures [59]. In the present study, both CO and NO2 levels are relatively higher in highly urbanized region and boomtown than in other areas (Table 3). Notably, both noise and air pollution may damage the cochlear HCs via oxidative stress [60], hypoxia-induced reactive oxygen species, and HC damage [48]. Although we found a statistically significant association between air pollution and subsequent SHL, the present study had the following limitations that need to be considered: (1) The noise levels in the studied area and the genetic variants in the studied subjects, which are considered as important risk factors for SHL, were not clarified in the present study, and without the noise-level data, the scope and significance of the study are limited. (2) The study conducted in the assigned residential area was according to the subject’s condition which was associated with the treatment of acute upper respiratory infections in a clinic or hospital, resulting in the underestimation of every subject’s exposure level to each air pollutant in the studied area. However, our findings are still significant and require further investigation. (3) In the present study, we used the ICD-9-CM codes 389.10–389.12 and 388.01 for data acquisition of age-related hearing loss and SHL. However, we did not include the ICD-9-CM codes of sudden hearing loss (388.02) and conductive hearing loss (389.00 and 389.06) considering that only 3.6% (2724 SHL subjects/75,767 subjects) of the subjects were identified as SHL patients in this study (Table 1).

5. Conclusions

In conclusion, we linked the national health database and air quality database to report NO2 and CO as risk factors for SHL. Our results indicate that the highest quartile of each pollutant could increase the risk of SHL by almost 1.63 and 1.45 fold, respectively. Notably, a mid-level exposure to NO2, but not CO, could also significantly contribute to SHL development by 1.40 fold.

Author Contributions

Conceptualization, Y.-C.H.; Formal analysis, K.-H.C., R.-H.C. and C.-L.L.; Funding acquisition, Y.-C.H., K.-H.C., S.C.-S.T.; Investigation, K.-H.C., S.C.-S.T., C.-Y.L., R.-H.C., H.-C.F., F.C.-F.L., C.-L.L. and Y.-C.H.; Methodology, K.-H.C., C.-Y.L., R.-H.C., H.-C.F. and F.C.-F.L.; Project administration, Y.-C.H.; Supervision, Y.-C.H.; Validation, K.-H.C. and C.-Y.L.; Writing—original draft, K.-H.C., S.C.-S.T. and Y.-C.H.; Writing—review and editing, K.-H.C., S.C.-S.T. and Y.-C.H. All authors have read and agreed to the published version of the manuscript.

Funding

We are thankful for the grants from the Ministry of Science and Technology (MOST) of the Taiwan Government (MOST 107-2314-B-715-004-MY3, MOST103-2314-B-715-001-MY2, MOST104-2314-B-715-003-MY3, MOST 105-2320-B-039-059-MY3, MOST 108-2320-B-039-013) and intramural research grants from Mackay Medical College (1052B07, 1051B23, 1061B09, 1071B12, 1081E03) and the China Medical University (CMU108-MF-49). This study was supported in part by the Taiwan Ministry of Health and Welfare Clinical Trial and Research Center of Excellence (MOHW105-TDU-B-212-133019), Tungs’ Taichung Metroharbor Hospital (TTMHH-109R0046), China Medical University Hospital, Drug Development Center, China Medical University from The Featured Areas Research Center Program within the framework of the Higher Education Sprout Project by the Ministry of Education (MOE), Academia Sinica Taiwan Biobank Stroke Biosignature Project (BM10501010037), NRPB Stroke Clinical Trial Consortium (MOST 104-2325-B-039-005), Tseng-Lien Lin Foundation, Taichung, Taiwan, Taiwan Brain Disease Foundation, Taipei, Taiwan, and Katsuzo and Kiyo Aoshima Memorial Funds, Japan. This study is supported in part by the Taiwan Ministry of Health and Welfare Clinical Trial Center (MOHW108-TDU-B-212-133004), China Medical University Hospital, Academia Sinica Stroke Biosignature Project (BM10701010021), MOST Clinical Trial Consortium for Stroke (MOST 108-2321-B-039-003-), Tseng-Lien Lin Foundation, Taichung, Taiwan, and Katsuzo and Kiyo Aoshima Memorial Funds, Japan.

Conflicts of Interest

The authors declare no conflict of interest

Data Availability

The authors confirm that all data underlying the findings are fully available without restriction. The dataset is owned by the Taiwan National Health Research Institutes (NHRI). Requests for the dataset may be sent via an e-mail to the NHRI at [email protected] or call at +886-037-246166 ext. 33603 for immediate service. Office Hours: Monday–Friday, 8:00–17:30 (UTC+8).

Abbreviations

AMDAge-related macular degeneration
COCarbon monoxide
LHIDLongitudinal Health Insurance Database
NHIRDNational Health Insurance Research Database
NHINational Health Insurance
NO2Nitrogen dioxide
PDParkinson’s disease
PM10Particulate matter 10
RNSReactive nitrogen species
SHLSensorineural hearing loss

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Figure 1. Probability free of SHL among three levels (Low, 2nd or High level) of pollutants concentrations: (a) CO; (b) NO2.
Figure 1. Probability free of SHL among three levels (Low, 2nd or High level) of pollutants concentrations: (a) CO; (b) NO2.
Ijerph 17 01969 g001
Table 1. Distribution of the demographic data of the study participants.
Table 1. Distribution of the demographic data of the study participants.
CovariatesCategoriesHearing Loss
(n = 2724)
Without Hearing Loss
(n = 73,043)
pTotal
(n = 75,767)
AgeMean (SD)60.8(11.6)53.9(11.0)<0.00154.1(11.1)
Follow yearsMean (SD)6.3(3.4)11.3(1.9)<0.00111.1(2.2)
Male 156957.632,79144.9<0.00134,36045.3
Insurance fee
(NTD)
>17,400114842.122,94831.4<0.00124,09631.8
17,400–19,20088432.525,68635.2 26,57035.1
>19,20069225.424,40933.4 25,10133.1
UrbanizationHighly81529.923,83832.6<0.00124,65332.5
Moderately92133.824,18633.1 25,10733.1
Boomtown36213.311,81716.2 12,17916.1
Others62623.013,20218.1 13,82818.3
COLow91833.724,80034.0<0.00125,71833.9
2nd71726.324,18733.1 24,90432.9
High108940.024,05632.9 25,14533.2
Mean (SD)0.72(0.27)0.71(0.27)0.3130.71(0.27)
NO2Low83430.626,17835.8<0.00127,01235.7
2nd90933.423,83932.6 24,74832.7
High98136.02302631.5 24,00731.7
Mean (SD)22.10(7.32)22.31(6,76)0.12922.31(6.78)
CO: carbon monoxide; NO2: nitrogen dioxide; NTD: new Taiwan dollar.
Table 2. Distribution of the comorbidities of the study participants.
Table 2. Distribution of the comorbidities of the study participants.
n, %Hearing Loss
(n = 2724)
Without Hearing Loss
(n = 73,043)
pTotal
(n = 75,767)
HT172863.441,81357.2<0.00143,54157.5
DM51919.115,10520.70.04215,62420.6
Stroke 2087.666839.10.00868919.1
Head injury2679.871359.80.98074029.8
CKD1395.138465.30.74239855.3
IHD120144.125,00734.2<0.00126,20834.6
Alcoholism261.010191.40.06410451.4
Nicotine321.215992.2<0.00116312.2
Asthma49518.212,77917.50.37513,27417.5
COPD120844.324,95434.2<0.00126,16234.5
RA110.43520.50.6613630.5
HT: hypertension; DM: diabetes mellitus; CKD: chronic kidney disease; IHD: ischemic heart disease; Nicotine: nicotine dependence; COPD: chronic obstructive pulmonary disease; RA: rheumatoid arthritis.
Table 3. Distributions of NO2 and CO among urbanization zones.
Table 3. Distributions of NO2 and CO among urbanization zones.
n, %Highly Urbanized
(n = 24,653)
Moderately Urbanized
(n = 25,107)
Boomtown
(n = 12,179)
Others
(n = 13,828)
Total
(n = 75,767)
COLow489119.8872934.8382831.4827059.825,71833.9
2nd671827.3922036.7505641.5391028.324,90432.9
High13,04452.9715828.5329527.1164811.925,14533.2
Mean (SD)0.82 (0.31)0.69 (0.24)0.71 (0.22)0.58 (0.21)0.71 (0.27)
NO2Low570923.2984139.2291223.9855061.827,01235.7
2nd585123.7933437.2562746.2393628.524,74832.7
High13,09353.1593223.6364029.913429.724,00731.7
Mean (SD)24.69 (6.65)21.83 (6.45)23.54 (5.33)17.87 (6.37)22.31 (6.78)
Table 4. Incidence and incidence rate ratio of hearing loss for the three levels of air pollutant exposure.
Table 4. Incidence and incidence rate ratio of hearing loss for the three levels of air pollutant exposure.
PollutantsLevelsn of HLFollow YearsIRIRR95%CI
COLow918287,4143.191.00
2nd717282,2562.540.790.72–0.88
High1089274,9083.961.241.14–1.36
NO2Low834304,5772.741.00
2nd909275,5993.301.211.10–1.32
High981264,4013.711.361.24–1.49
PY: person-years; n of HL: number of patients with hearing loss; IR: incidence rate (per 1000 person-years); IRR: incidence rate ratio.
Table 5. Adjusted HR of hearing loss in the moderate and high concentration groups compared to that in the low concentration group.
Table 5. Adjusted HR of hearing loss in the moderate and high concentration groups compared to that in the low concentration group.
PollutantsLevelsAllSex-Specific RiskAge-Specific Risk
Adjusted HR95%CIpAdjusted HR95%CIpAdjusted HR95%CIp
COcontinuous1.351.17–1.56<0.0011.25male1.03–1.52<0.0011.30<=500.97–1.740.084
2nd versus Low0.900.82–1.000.0500.88male 0.77–1.010.0641.00<=500.81–1.230.995
High versus Low1.451.31–1.59<0.0011.38male 1.22–1.57<0.0011.65<=501.35–2.03<0.001
continuous 1.49female1.20–1.85<0.0011.37>501.17–1.62<0.001
2nd versus Low 0.94female0.81–1.100.4590.88>500.79–0.990.034
High versus Low 1.53female1.32–1.77<0.0011.394>501.25–1.55<0.001
NO2continuous1.011.001–1.010.0241.01male1.00–1.010.2151.01<=501.00–1.020.168
2nd versus Low1.401.27–1.54<0.0011.38male1.21–1.56<0.0011.45<=501.18–1.79<0.001
High versus Low1.631.48–1.81<0.0011.56male1.36–1.78<0.0011.92<=501.55–2.37<0.001
continuous 1.01female1.001–1.020.0311.01>501.00–1.010.057
2nd versus Low 1.41female1.22–1.64<0.0011.39>501.25–1.55<0.001
High versus Low 1.73female1.49–2.02<0.0011.56>501.40–1.75<0.001
Adjusted HR: adjusted hazard ratio in the multivariate analysis after adjusting for age, sex, insurance fee, urbanization, HT, DM, stroke, head injury, CKD, IHD, alcoholism, nicotine dependence, asthma, and COPD.
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