Long-Term Exposure to Air Pollution and The Risk of Developing Sudden Sensorineural Hearing Loss

doi:10.21203/rs.3.rs-72326/v1

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Long-Term Exposure to Air Pollution and The Risk of Developing Sudden Sensorineural Hearing Loss

https://doi.org/10.21203/rs.3.rs-72326/v1

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published 11 Oct, 2021

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Background The association between exposure to air pollution and sudden sensorineural hearing loss (SSNHL) has not been extensively discussed in the literature. Therefore, we conducted this nationwide study to evaluate the risk of SSNHL in Taiwanese residents with exposure to air pollution.

Methods We enrolled subjects aged older than 20 years with no history of SSNHL from 1998 to 2010, and followed up until developing SSNHL, withdrawn from the National Health Insurance program, and the end of the database (2011/12/31). The air quality data are managed by Taiwan Environmental Protection Administration. The annual concentrations of PM_2.5, SO₂, CO, NO, and NO₂ from 1998 to 2010 were classified into the three levels according to tertiles. We calculated the annual average of pollutants from baseline until the end of the study, and classified into tertiles. The adjusted hazard ratio (aHR) was estimated by using the multivariate Cox proportional hazard model.

Results When considered continuous air pollutants concentration, subjects who exposed with higher concentration of CO (aHR=2.19, 95%CI=1.52-3.15), NO (aHR=1.02, 95%CI=1.01-1.03), and NO₂ (aHR=1.02, 95%CI=1.01-1.04) developing significant higher risk of SSNHL.When classified air pollutants concentration into low, moderate and high level by tertiles, and selected low level as reference, patients exposed with moderate (aHR=1.58, 95%CI=1.21-2.06) or high level (aHR=1.32, 95%CI=1.00-1.74) of PM_2.5 showed significant higher risk of developing SSNHL.

Conclusion This study indicated an increased risk of SSNHL in residents with long-term exposure to air pollution. Nevertheless, further experimental and clinical studies are needed to validate the study findings.

Disclosure statement

All authors declare that there is no conflicts of interest. This study was approved in part by Taiwan Ministry of Health and Welfare Clinical Trial and Research Center of Excellence (MOHW105-TDU-B-212-133019). The committee agree to waive the requirement for consent.

Translational Medicine

air pollution

sudden sensorineural hearing loss (SSNHL)

adjusted hazard ratio (aHR)

National Health Insurance program.

Air pollution has become an important environmental issue in the last decade, especiallyin the developing and developed countries. The levels of air pollutants are highly and positively correlated with population density, vehicle emissions, agriculture, industrial emissions, power plants, and fossil fuel combustion.(1, 2) Exposure to air pollutants triggers systemic and tissue-specific inflammation.(3, 4)Previous studies have indicated that exposure to air pollutionincreases the risks of degeneration diseases, cerebrovascular and cardiovascular diseases, immunological diseases, malignant tumors, and ophthalmological diseases.(5–12). In addition, air pollution is the major environment-related risk factor forhuman mortality.(13)

Although viral infection, environmental or occupational factors (such asloud noises, heavy metals, and organic solvents), autoimmune diseases, cardiovascular diseases,accidental events, endothelial dysfunction,metabolic diseases, and health habits (such as smoking and alcohol consumption)are risk factors for sudden deafness (sudden sensorineural hearing loss,SSNHL), the complex etiology of SSNHL remains unclear.(14–23)Exposure to air pollution increases oxidative stress, which can play an important role in endothelial dysfunction.(24)A previous studyreports air pollution as a risk factor ofdeveloping sensorineural hearing loss.(25)However, the association between exposure to air pollution and SSNHL has not been extensively discussed in the literature. Therefore, we conducted this nationwide study to evaluate the risk of SSNHL in Taiwanese residents with exposure to air pollution.

Data Source and Study Subjects

Taiwan government built a nationwide database, named National Health Insurance Database (NHIRD),since 1995and included the medical record of health insurance single payer in Taiwan. The medical record included the history of outpatients, hospitalization, the prescriptions of medications and other medical services. As of today, more than 99% of Taiwan population were enrolled in the database. We conducted this study by Longitudinal Health Insurance Database (LHID 2000), which was randomly selected 1 million study subjects from NHIRD. All identification number were encrypted for the patients’ privacy. The history diagnoses are coded according to the International Classification of Disease, Ninth Revision, Clinical Modification (ICD-9-CM). The Research Ethics Committee of China Medical University and Hospital in Taiwan approved the study (CMUH-104-REC2-115-R4).

We enrolled subjects aged older than 20 years with no history of SSNHL from 1998 to 2010, and followed up until developing SSNHL, withdrawn from the NHI program, and the end of the database (2011/12/31).

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 PM_2.5, SO₂, CO, NO, and NO₂ from 1998 to 2010 were classified into the three levels according to tertiles: the PM_2.5 concentrationsof the low-, mid-, and high-level groups were<30.29 (μg/m³), 30.29-37.61 (μg/m³) and >37.61 (μg/m³), respectively.the SO₂ concentrationsof the low-, mid-, and high-level groups were<3.57 (ppb), 3.57-5.51 (ppb) and >5.51 (ppb), respectively.the CO concentrationsof the low-, mid-, and high-level groups were<0.61 (ppm), 0.61-0.76 (ppm) and >0.76 (ppm)respectively.the NO concentrationsof the low-, mid-, and high-level groups were<5.04 (ppb), 5.04-8.90 (ppb) and >8.90 (ppb), respectively.the NO₂ concentrationsof the low-, mid-, and high-level groups were<19.48 (ppb), 19.48-25.55 (ppb) and >25.55 (ppb), respectively.

Main Outcome and Covariates

The main outcome of this study was the SSNHL (ICD-9-CM: 3882; ICD-10-CM: H91.20, H91.21, H91.22, H91.23). The demographic factors we considered included age, insurance fee, urbanization and comorbidities. The common comorbidities including hypertension (HT, ICD-9-CM codes 401–405), diabetes mellitus (DM, ICD-9-CM code250), stroke, head injury (ICD-9-CM codes 850–854), chronic kidney disease (CKD, ICD-9-CM code 585), ischemic heart disease (IHD, ICD-9-CM codes 410–414), alcoholism (ICD-9-CM codes305.0 and 303), asthma(ICD-9-CM code493), Chronic obstructive pulmonary disease (COPD, ICD-9-CM codes 490–492, 494, and 496), andrheumatoid arthritis(RA, ICD-9-CM code 714)were presented as confounding factors in this study.

Statistical Analysis

We presented continuous variables by mean and standard deviation; categorical variables were shown by number and percentage. The difference between with and without SSNHL were tested by t-test and chi-square test for continuous and categorical variable, respectively. To analyze the exposures across the long-term period, we calculated the annual average of pollutants from baseline until the end of the study, and classified into tertiles: the low, moderate, and high-level groups. When compared mean and classified pollutants concentration in four level of urbanization (highly, moderately, boomtown and others), ANOVA test and chi-square test was applied, respectively.

The incidence rates of SSNHL were calculated, and the hazard ratio (HR) was estimated by using the multivariate Cox proportional hazard model, adjusting for age, sex, insurance fee, urbanization, and comorbidities.

We totally enrolled 64,321 subjects in this study. 353 with SSNHL and the other 63,968 without SSNHL. Table 1 presented the distribution of demographics and comorbidities between two groups. The mean age of SSNHL and non-SSNHL were 45.58 and 39.12 years, and with 8.47 and 11.71 follow up years, respectively. Patients with SSNHL had significant higher percentage of HT (45.6%), DM (17.3%), IHD (27.5%), andCOPD (29.5%) then non-SSNHL group. The distribution of the levels of insurance fee showed insignificant between two groups. Most study subjects lived in highly (34.3%) and moderately (32.6%) urbanized area.Table 2 showed the distribution of different pollutants concentration and SSNHL. SO₂ and NO₂ concentration showed insignificant difference between SSNHL and non-SSNHL group when calculated by mean or classified into levels.The mean of CO (0.76 vs 0.72) and NO (12.6 vs 11.0) concentration was significant higher in the group of SSNHL, respectively.Table 3 showed the association between pollutants concentration and urbanized level. The level of CO, NO and NO₂ showed the mean 0.81, 0.69, 0.70 and 0.59 (ppm); 14.14, 9.94, 10.73 and 6.80 (ppb); 24.58, 22.06, 23.39, and 18.63 (ppb) from highly urbanized, moderately, boomtown to others, respectively. The pollutants we mentioned above might highly associated with the level of urbanization.The risk of SSNHL and the level of air pollutants were calculated in Table 4.When considered continuous air pollutants concentration, subjects who exposed with higher concentration of CO (adjusted hazard ratio (aHR) = 2.19, 95%CI = 1.52–3.15), NO (aHR = 1.02, 95%CI = 1.01–1.03), and NO₂ (aHR = 1.02, 95%CI = 1.01–1.04) developing significant higher risk of SSNHL.When classified air pollutants concentration into low, moderate and high level by tertiles, and selected low level as reference, patients exposed with moderate (aHR = 1.58, 95%CI = 1.21–2.06) or high level (aHR = 1.32, 95%CI = 1.00-1.74) of PM_2.5 showed significant higher risk of developing SSNHL.

Table 1

Distribution of the demographic data and comorbidities of the study participants.
Covariates		SSNHL (n = 353)		Non- SSNHL (n = 63968)		p	Total (n = 64321)
Age	Mean (SD)	45.58 (15.36)		39.12 (14.99)		< 0.001	39.16 (15.00)
follow years	Mean (SD)	8.47 (2.49)		11.71 (0.91)		< 0.001	11.69 (0.96)
HT		161	45.6%	19464	30.4%	< 0.001	19625	30.5
DM		61	17.3%	7023	11.0%	< 0.001	7084	11.0
Stroke		19	5.4%	2586	4.0%	0.255	2605	4.0
Head injury		27	7.6%	5237	8.2%	0.787	5264	8.2
CKD		10	2.8%	1584	2.5%	0.796	1594	2.5
IHD		97	27.5%	10776	16.8%	< 0.001	10873	16.9
Alcoholism		7	2.0%	975	1.5%	0.629	982	1.5
Nicotine		5	1.4%	1814	2.8%	0.149	1819	2.8
Asthma		50	14.2%	7581	11.9%	0.208	7631	11.9
COPD		104	29.5%	13997	21.9%	0.001	14101	21.9
RA		1	0.3%	191	0.3%	1.000	192	.3
Insurance fee	Lowest	59	16.7%	10633	16.6%	0.316	10692	16.6
	2nd	102	28.9%	20987	32.8%		21089	32.8
	3rd	91	25.8%	14280	22.3%		14371	22.3
	Highest	101	28.6%	18068	28.2%		18169	28.2
Urbanization	Highly	108	30.6%	21946	34.3%	0.002	22054	34.3
	Moderately	138	39.1%	20837	32.6%		20975	32.6
	Boomtown	40	11.3%	10856	17.0%		10896	16.9
	Others	67	19.0%	10329	16.1%		10396	16.2
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 2

Distribution of air pollutant exposure in study participants.
Pollutants	Levels	SSNHL (n = 353)		Non- SSNHL (n = 63968)		p	Total (n = 64321)
PM_2.5 (µg/m³)	Mean (SD)	35.07 (8.74)		34.79 (8.75)		0.556	34.79 (8.75)
	Low	92	26.1%	21393	33.4%	0.007	21485	33.4
	Moderate	133	37.7%	20202	31.6%		20335	31.6
	High	128	36.3%	22373	35.0%		22501	35.0
SO₂ (ppb)	Mean (SD)	4.91 (2.50)		4.98 (2.41)		0.557	4.98 (2.41)
	Low	127	36.0%	21641	33.8%	0.519	21768	33.8
	Moderate	111	31.4%	19691	30.8%		19802	30.8
	High	115	32.6%	22636	35.4%		22751	35.4
CO (ppm)	Mean (SD)	0.76 (0.33)		0.72 (0.27)		0.010	0.72 (0.27)
	Low	124	35.1%	22582	35.3%	0.204	22706	35.3
	Moderate	93	26.3%	19242	30.1%		19335	30.1
	High	136	38.5%	22144	34.6%		22280	34.6
NO (ppb)	Mean (SD)	12.60 (12.70)		11.00 (10.13)		< 0.001	11.01 (10.15)
	Low	119	33.7%	21754	34.0%	0.936	21873	34.0
	Moderate	109	30.9%	20140	31.5%		20249	31.5
	High	125	35.4%	22074	34.5%		22199	34.5
NO₂ (ppb)	Mean (SD)	22.99 (7.49)		22.56 (6.55)		0.216	22.56 (6.56)
	Low	114	32.3%	20002	31.3%	0.156	20116	31.3
	Moderate	101	28.6%	21284	33.3%		21385	33.2
	High	138	39.1%	22682	35.5%		22820	35.5
SD: standard deviation; ppb: parts per billion; ppm: parts per million

Table 3

Distributions of air pollutants among urbanization zones.
Pollutants	Levels	Highly Urbanized (n = 22054)		Moderately Urbanized (n = 22975)		Boomtown (n = 10896)		Others (n = 10396)		p	Total (n = 64321)
PM_2.5 (µg/m³)	Mean (SD)	32.71 (7.85)		35.68 (9.16)		37.24 (8.44)		34.86 (9.04)		< 0.001	34.79 (8.75)
	Low	9906	44.9	6335	30.2	2651	24.3	2593	24.9	< 0.001	21485	33.4
	Moderate	7680	34.8	6067	28.9	3538	32.5	3050	29.3		20335	31.6
	High	4468	20.3	8573	40.9	4707	43.2	4753	45.7		22501	35.0
SO₂ (ppb)	Mean (SD)	4.88 (2.09)		5.23 (2.53)		5.76 (2.74)		3.86 (1.97)		< 0.001	4.98 (2.41)
	Low	7275	33.0	6100	29.1	2700	24.8	5693	54.8	< 0.001	21768	33.8
	Moderate	6833	31.0	6737	32.1	3233	29.7	2999	28.8		19802	30.8
	High	7946	36.0	8138	38.8	4963	45.5	1704	16.4		22751	35.4
CO (ppm)	Mean (SD)	0.81 (0.30)		0.69 (0.24)		0.70 (0.22)		0.59 (0.21)		< 0.001	0.72 (0.27)
	Low	5516	25.0	7839	37.4	3492	32.0	5859	56.4	< 0.001	22706	35.3
	Moderate	4810	21.8	6904	32.9	4534	41.6	3087	29.7		19335	30.1
	High	11728	53.2	6232	29.7	2870	26.3	1450	13.9		22280	34.6
NO (ppb)	Mean (SD)	14.14 (12.66)		9.94 (8.21)		10.73 (8.43)		6.80 (6.75)		< 0.001	11.01 (10.15)
	Low	4156	18.8	7342	35.0	3177	29.2	7198	69.2	< 0.001	21873	34.0
	Moderate	6556	29.7	7551	36.0	4205	38.6	1937	18.6		20249	31.5
	High	11342	51.4	6082	29.0	3514	32.3	1261	12.1		22199	34.5
NO₂ (ppb)	Mean (SD)	24.58 (6.51)		22.06 (6.30)		23.39 (5.19)		18.43 (6.41)		< 0.001	22.56 (6.56)
	Low	4245	19.2	7283	34.7	2547	23.4	6041	58.1	< 0.001	20116	31.3
	Moderate	6127	27.8	7354	35.1	4930	45.2	2974	28.6		21385	33.2
	High	11682	53.0	6338	30.2	3419	31.4	1381	13.3		22820	35.5
ppb: parts per billion; ppm: parts per million

Table 4

Adjusted HR of SSNHL in the moderate and high concentration groups compared to the values in the low concentration group.
Pollutants	Levels	n of SSNHL	Person-Years	IR	aHR	95%CI		p
PM_2.5 (µg/m³)	Continuous				1.01	0.99	1.02	0.368
	Low	92	251573	0.37	Reference
	Moderate	133	238157	0.56	1.58	1.21	2.06	0.001
	High	128	262340	0.49	1.32	1.003	1.74	0.048
SO₂ (ppb)	Continuous				1.00	0.96	1.05	0.914
	Low	127	253994	0.50	Reference
	Moderate	111	231810	0.48	1.01	0.78	1.31	0.923
	High	115	266267	0.43	0.94	0.73	1.23	0.669
CO (ppm)	Continuous				2.19	1.52	3.15	< 0.001
	Low	124	265999	0.47	Reference
	Moderate	93	226689	0.41	0.96	0.73	1.27	0.795
	High	136	259382	0.52	1.28	0.99	1.65	0.063
NO (ppb)	Continuous				1.02	1.01	1.03	< 0.001
	Low	119	255830	0.47	Reference
	Moderate	109	237175	0.46	1.14	0.87	1.49	0.354
	High	125	259066	0.48	1.22	0.93	1.60	0.157
NO₂ (ppb)	Continuous				1.02	1.01	1.04	0.010
	Low	114	235391	0.48	Reference
	Moderate	101	250758	0.40	0.94	0.72	1.24	0.671
	High	138	265922	0.52	1.25	0.96	1.63	0.100
n of SSNHL: number of patients with hearing loss; IR: incidence rate (per 1000 person-years); IR: incidence rate; aHR: adjusted hazard ratio in the multivariate analysis after adjusting for age, insurance fee, urbanization, HT, DM, stroke, head injury, CKD, IHD, alcoholism, nicotine dependence, COPD, asthma, RA.

This retrospective cohort study combined two large, longitudinal databases to evaluate the risk of SSNHL in Taiwanese residents with chronic exposure to air pollution.During the approximately 11-year follow-up, we enrolled 64,321 residents (353 in SSNHL; 63,968 in non-SSNHL) and found the participants who were exposed to PM_2.5, CO, NO, and NO₂had a significantly higher risk of SSNHL.However, SO₂ exposure was not similarly correlated.

The association between exposure to air pollution and development of hearing lossis unclear. In 2019, a nested case-control indicatedthat short-term exposure to NO₂ significantly increased the risk of SSNHL (adjusted odds ratio: 3.12 [95%confidence interval: 2.16–4.49)].(26)Another large scale study in Korea found a weak relationship between daily numbers of SSNHL patients and PM levels (27). Nevertheless, the association between long-term exposure to air pollution and development of SSNHL remains debatable and requires further clarification.

According to Table 3, the distributions of PM_2.5 and SO₂ were not consistent with urbanization levels. This discrepancy may result from intensive agricultural activities in the less urbanized cities.(28–30)Fossil fuel combustion in industrial facilities or power plants isthe major source of SO₂ emissions.(31)Because of the high land value and appropriateland and emission standards, industrial factories or power plants are not preferably setup in areas with a high population density.

This nationwide study withminimized selection bias has several limitations. First, we considered the medical convenience; thus,the definition of residential address was based on the location of medical institutions where participants most frequently received therapy for acute respiratory infections. According to this definition,there was a potential bias ofexcluding subjects without related medical records. However, evidence indicates that these people most likely had less air pollutant exposure.(32–34) This may result in an underestimation of SSNHL cases. Second, SSNHL is anemergency otologic condition. There were more frequent hospital visits by residents in highly urbanized cities with high levels of air pollutants than other areas. Although this may result in surveillance bias and an overestimation of the risk of SSNHL,previous evidence indicates the obvious narrowing of health disparities between urban and rural areasbecause of the NHI program removing some barriers and providingfree health care in the less urbanized areas.(35, 36)Third, althoughthe records of SSNHL were acquiredaccording to the claim data from the NHIRD instead ofby physical examination, the SSNHL diagnosis was validated by audiology examinations and neurological findings to avoid strict fines from Taiwan Bureau of National Health Insurance. Fourth,patients’ occupation and health behaviors, such as smoking and alcohol consumption,which are considered risk factors of SSNHL,were not available from the NHIRD. Hence, we considered insurance fees, COPD, asthma, nicotine dependence, and alcoholism in themultivariate analysis. Smoking behavior was highly correlated with the development of COPD and asthma.(37–40) The diagnosis of alcoholism was according to patients' attitudes and drinking behaviors.(41)In severalprevious NHIRD-related studies, COPD, asthma, nicotine dependence, and alcoholism were considered risk factors instead of smoking and drinking.(42–44)Fifth, traffic-related air pollutants co-occur with noise. It is not feasible to clarify the contributions of air pollution and noise individually due to the lack of noise data in the two large databases. Therefore, the application of the present study is limited. Despite these limitations, the present nationwide study with a long follow-up period might reduce the impacts of biases.

In conclusion, we redefined the residential area by the location of hospital or clinics rather than the addresses of group insurance applicants and considered the proxy covariates of health behaviors to overcome the inherent limitation of the NHIRD. This study indicated an increased risk of SSNHL in residents with exposure to air pollution. Nevertheless, further experimental and clinical studies are needed to validate the study findings.

Acknowledgements

We thank the grant supports from the following sources: Tung’s Taichung MetroHarbor hospital research grant (TTMHH-R1100012); Taiwan Ministry of Health and Welfare Clinical Trial and Research Center of Excellence (MOHW104-TDU-B-212-113002); China Medical University Hospital, Academia Sinica Taiwan Biobank, Stroke Biosignature Project (BM104010092); NRPB Stroke Clinical Trial Consortium (MOST 103-2325-B-039 -006); Tseng-Lien Lin Foundation, Taichung, Taiwan; Taiwan Brain Disease Foundation, Taipei, Taiwan; Katsuzo and Kiyo Aoshima Memorial Funds, Japan; and CMU under the Aim for Top University Plan of the Ministry of Education, Taiwan.

Ethics approval and consent to participate

This study was approved by the Ethics Review Board of China Medical University and Hospital, Taiwan (CMUH-104-REC2-115). The IRB waived the consent requirement.

Consent for publication

Not applicable.

Availability of data and materials

Data are available from the NHIRD published by Taiwan National Health Insurance Bureau. Due to the ‘Personal Information Protection Act’, data cannot be made publicly available (http://nhird.nhri.org.tw/en/index.html).

Competing interests

The authors declare that they have no competing interests.

Funding

This study is supported in part by Taiwan Ministry of Health and Welfare Clinical Trial Center (MOHW109-TDU-B-212-114004), MOST Clinical Trial Consortium for Stroke (MOST 108-2321-B-039-003-), Tseng-Lien Lin Foundation, and Tungs’ Taichung Metroharbor Hospital (TTMHH-R1100012).

Authors' contributors

Conceptualization: K-HC; methodology: K-HC, C-LL; formal analysis: K-HC and C-LL; investigation: all authors; writing (original draft preparation): K-HC; writing (review and editing):all authors; visualization: all authors; supervision: K-HC; project administration: K-HC.

Acknowledgements

We thank the staff of the Management Office for Health Data of China Medical University Hospital for their contributions to this study.

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Long-Term Exposure to Air Pollution and The Risk of Developing Sudden Sensorineural Hearing Loss

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