|Year : 2012 | Volume
| Issue : 4 | Page : 268-273
Respiratory morbidity in spray paint workers in an automobile sector
Savitri P Siddanagoudra1, Dasannanmalige H Kanyakumari2, Santhebachahalli M Nataraj3
1 Department of Physiology, SDM College of Medical Sciences and Hospital, Dharwad, India
2 Department of Physiology, BMC and Hospital Chitradurga, Karnataka, India
3 Department of Physiology, JSS MC and Hospital (JSS University), Mysore, Karnataka, India
|Date of Web Publication||27-Feb-2013|
Savitri P Siddanagoudra
Department of Physiology, SDM College of Medical Sciences and Hospital, Dharwad, d/o Shri P. C. Siddanagoudra, H.No 91 7th cross, Vishweshwar Nagar, Hubli, Karnataka
Source of Support: None, Conflict of Interest: None
Background: Occupational asthma (OA) is a major cause of respiratory morbidity and the most common cause of non-acute lung disease in the industrialized world. The incidence of OA in developed country is increasing, while in developing countries is still unknown. Automobile industry is a place where workers are exposed to harmful chemicals and toxic substances. In automobile industry work floor assembly lines chassis move continuously and pass by "Robot Painter" that spray them and workers assemble the chassis. The paint that is used contains isocyanate (low-molecular-weight compound) which is most common agent responsible for OA. Objective: The present study is undertaken to assess respiratory morbidity of paint workers in terms of obstructive and restrictive lung pattern and to study relationship between duration of exposure and respiratory morbidity. Materials and Methods: This cross-sectional study included 70 car spray paint workers, who are working for 1-6 years in an automobile industry. A pre-structured questionnaire was used to record the clinical, sociodemographic profile, and clinical examination. Pulmonary function parameters were recorded by a computerized spirometer-Medspiror during their working hours. An independent t test and a correlation test were applied. Results: Sixty-one workers had normal lung functions. The nine isocyanate-exposed workers showed a significant reduction in FEV 1 /FVC (P < 0.05) suggestive of obstructive lung pattern. There is a strong correlation between duration of exposure and pulmonary functions (P value = 0.002). Conclusion: Decreased pulmonary function tests (PFT) in spray painters were related to duration of exposure to isocyanate.
Keywords: Isocyanate (spray paint), isocyanate-induced asthma, respiratory morbidity preventive measures
|How to cite this article:|
Siddanagoudra SP, Kanyakumari DH, Nataraj SM. Respiratory morbidity in spray paint workers in an automobile sector. Int J Health Allied Sci 2012;1:268-73
|How to cite this URL:|
Siddanagoudra SP, Kanyakumari DH, Nataraj SM. Respiratory morbidity in spray paint workers in an automobile sector. Int J Health Allied Sci [serial online] 2012 [cited 2021 Apr 23];1:268-73. Available from: https://www.ijhas.in/text.asp?2012/1/4/268/107897
| Introduction|| |
Occupational asthma (OA) is defined as asthma caused or made substantially worse by agents inhaled in the occupational environment.  Diisocyanates have been the most commonly identified causing agent for OA in industrialized areas. Asthma among diisocyanate-exposed workers is due to a high level of irritant exposure at work or by sensitization to diisocyanates. Alternatively, asthma may be coincidental or may be aggravated by work exposure.  Risk of occupational exposure to isocyanates is increasing substantially because of the rapidly expanding use of coating materials (paints), polyurethane foam manufacturing, and binders. , Spray paint contains isocyanate a low-molecular-weight compound. Spray painting is a process by which exposure to isocyanates can be high. These spray paint creates fine mists or droplets of paint that may stay suspended in the air for a short period of time there by increasing the risk of inhalation and eye, skin exposure.  Some examples for diisocyanates are TDI (toluene diisocyanate), MDI (methylene diphenyl diisocyanate), HDI (hexamethylene diisocyanate).
Since Fuchs and Valade were the first to recognize that isocyanate exposure can cause respiratory diseases, numerous studies have been carried out among paint works.  In recent years, many studies documented the effects of spray painton respiratory functions. Compared with OA caused by other agents, those with OA due to diisocyanates had a significantly earlier onset of asthma (mean 5 years vs. 7 years). ,
The early identification of OA in workers lead to reversal of the symptoms and prevent additional workers from being at risk of getting OA. Without early detection, workers will be needlessly put at risk of developing morbid lung diseases possibly preventing from enjoying leisure sports activities and continuing to work in the same profession.  Despite possible adverse health effects, there has been little epidemiologic investigations of the automobile repair industry in developing countries.  Hence, the present study was aimed to assess the respiratory morbidity in spray paint workers by recording pulmonary function tests (PFTs).
| Materials and Methods|| |
The present study was designed as a cross-sectional study. Prior to the commencement of the study, the ethical clearance was taken from the J.S.S Medical College, Mysore. A study was carried out in an automobile shop in Bangalore city. A total of 70 male workers who were working in a car spray paint booth (exposed to diisocyanates) for 1-6 years and aged between 25 and 35 years were included. Among 110 workers in industry, only 70 were selected based on exclusion criteria. The informed written consent was taken from each subject.
Questionnaire for study group
Questionnaires were administered by author in Kannada language. An interview technique was used as a tool for data collection. Clinical history like history of breathlessness, chest tightness, cough, wheezing before or after employment, nocturnal awakening in the last year, symptoms regression on weekend or regression on holidays, family history of asthma, occupational rhinitis, dermatitis were asked. Occupational history about their previous job, present job was noted. For all 70 workers this was the first job and was no history about change of job. Sociodemographic history and clinical examination of the subjects were recorded on predesigned proforma.
Workers with previous exposure to any occupational exposure, diagnosed case of asthma or the symptoms suggested of asthma before joining the present job and any systemic illness.
In accordance with American College of Chest Physicians, we diagnosed OA and likely OA as follows: (A) diagnosis of asthma and (B) onset of asthma after entering the workplace: (C) association between symptoms of asthma and work, and (D) one or more of the following: (1) workplace exposure to an agent known to give rise to OA, (2) work-related changes in PEFR, (3) work-related changes in bronchial responsiveness, (4) positive response to specific inhalation test. 
OA: meets A + B + C + D2 or D3 or D4 of the surveillance case definition.
Likely OA: meets A + B + C + D1 only of the surveillance case definition.
Anthropometric measurement were recorded. PFT parameters were recorded by a computerized spirometer-Medspiror during their working hour. These are
Forced Vital Capacity (FVC).
Forced Expiratory Volume in First second (FEV 1 ).
FEV 1 /FVC (FEV 1 %).
Peak Expiratory Flow Rate (PEFR).
Forced Expiratory Flow during 25-75% expiration (FEF 25-75% ).
The subjects were familiarized with the set up and detailed instructions and demonstrations were given by the author. The subjects were made to breath out forcefully following deep inspiration into the mouth piece attached to the pneumotachometer. Expiration was maintained for a minimum period of 3-4 seconds. The American Thoracic Society (ATS) recommends that at least three acceptable maneuvers be saved. Among these three, the largest FVC must not vary more than 0.2 L or 5% from the second largest. Also largest FEV 1 must not vary more than 0.2 L or 5% from the second largest because this amount of variation can be seen within 1 day in normal subjects. Of these three maneuvers, the largest FVC and largest FEV 1 is reported. A normal PEFR value of 3-5 L/s ensured maximum effort by the subject while performing the test. Normal % predicted was taken as 80% according to ATS.  [Table 1] shows the interpretation of spirometry values.
All the recording were done at the body temperature and pressure saturated with water vapor concentration (BTPS). As recommended by Snowbird workshop all the readings were taken in standing position. All the tests were carried out at the same time of the day, between 8.30 am and 9.30 am to avoid possible variations. The tests were done in a quiet room in order to alleviate the emotional and psychological stresses. During the test, maximum effort from the subjects was ensured by adequately motivating them to perform at their optimum level. These above said parameters were compared with average predicted value for a subject on the basis ofage, sex, built andrace.  The Indian standard predicted values were taken for the calculation.
Spirometry is required for the evaluation of workers for disability under the Social Security Administration (SSA).  Occupational Safety and Health Administration (OSHA)  and in Workers Compensation Settings. 
Statistical analysis was performed using the Statistical Package for Social Sciences (SPSS-17). The results were expressed as mean ± standard deviation (SD). Independent t test was applied to study the PFTs in smokers and non-smokers and also for worker with symptoms suggestive of OA and without OA. Relationship between duration of exposure andrespiratory morbidity state was studied by correlation test. P < 0.05 was considered significant (S).
| Results|| |
Seventy spray paint workers based on the inclusion and exclusion criteria, were participated in the study. All the workers were males. Anthropometric and demographic characteristics of workers are depicted in [Table 2]. Mean and SD of age, height, weight and BMI was calculated. [Table 3] shows the occupational characteristics includes duration of exposure to automobile spray painting and smoking characteristics of workers. [Table 4] depicts respiratory symptoms of workers. Out of 70 workers, 65 had various symptoms listed in the [Table 4]. 3% of the workers had itching, redness, and swelling of skin. The scientific literature contains a limited amount of data suggesting that dermal exposure to diisocyanate may produce respiratory sensitization.  The PFTs of these workers were normal. [Table 5] shows PFTs results in which all the parameters (M ± SD) were normal compared to their % predicted. Statistically non-significant results as P value was > 0.05. But 9 workers had obstructive lung pattern when compared to their individuals % predicted. [Table 6] shows that out of 9 workers with obstruction 8 were smokers and 1 was nonsmoker. Based on clinical symptoms among 65 symptomatic workers, 9 had obstruction. In [Table 7], the independent t test was applied to measure the significance difference in PFTs values between workers with symptom, without symptom and between smoker and, non-smokers. There was non-significant difference in the PFTs for both the variables. Between workers with symptom, without symptom and between smokers and non-smokers, the P value was >0.05 and the t value with degree of freedom (df) was >0.05. [Figure 1] and [Figure 2], scatter diagrams, show the linear negative correlation between duration of exposure with FVC and with FEV1 respectively. Correlation was statistically significant at the 0.001 level (two-tailed) r = -.371 for FVC and -.365 for FEV1.
|Table 3: Occupational (includes duration of exposure to automobile spray painting) and smoking characteristics of workers|
Click here to view
|Table 7: Respiratory morbidity in workers with smoking history and symptomatology|
Click here to view
| Discussion|| |
An extensive amount of clinical/epidemiological literature exists regarding the effects of diisocyanate exposure on respiratory health. The key respiratory disorders examined are bronchial asthma and an accelerated decline in lung functions. OA is a disease characterized by increased airway responsiveness to a wide variety of both specific and non-specific stimuli in work place. The present study was an indoor-based air pollution problem in an automobile industry. This study revealed that nine spray painters showed < 70% FEV 1 /FVC suggestive of early obstructive lung disease when compared to their % predicted. PEFR and FEF 25-75% were also declined but not statistically significant suggesting smaller airway obstruction. All the nine workers had typical symptoms of OA. Among nine, seven were working for more than 5 years and two for 3-4 years and eight were smokers, one was non-smokers. This could be attributed to long duration of exposure to isocyanate. The Pearson correlation test showed negative correlation which concludes, as duration of exposure increases the PFTs decreases. Compared to non-smokers the smokers PFTs were not statistically declined. This needs a further study with large sample for statistical significance. The difference in PFTs between workers with symptoms and without symptoms were not significant statistically, could be due to acute sensitization (lesser duration of exposure) in which the PFTs will remain normal.
The present study is in harmony with previous studies. In a similar study by Schwarz and Baker concluded that increased risk of airflow obstruction in painters was related to duration of exposure to isocyanate and was independent of the effects of cigarette smoking.  It was shown in a 2.5 years follow-up study that, the PFTs of workers exposed to isocyanate for longer duration, were reduced even in very low concentration. 
Similar correlation between higher exposure to TDI and larger annual decline in FEV 1 , FVC and FEF 25-75% in painters was shown in a longitudinal study of 5 years. , In this study, we enquired regarding the proper designing of paint booth and use of preventive measures by workers which were under standard. It was reported in a study that despite of improvements in autobody shop materials, practices, and control, there are still opportunities for substantial exposure to isocyanates on long terms.  It was shown by Mapp CE and others in their study that paint workers developed asthmatic reaction after exposure to isocyanate.  A follow-up study for 6 years was conducted in which the impairment correlated well with the frequency of high peak exposure to HDI, not with the mean exposure to diisocyanate.  It was concluded in a study that OA is common disorder among automobile painters and duration of exposure as significant effects on OA occurrence. , A study found the correlation between FVC within the week and the long-term (6 years) changes in FVC, standardized for the effects of smoking and exposure.  Years working in a non-functioning paint booth, along with smoking, were associated with in the low FEV 1 /FVCindicating obstructive diseases of lung. 
Since chemicals with MW less than 1000 daltons cause rarely antigenic, but may act as haptens. It has been proved that isocyanate act as pharmacologic inhibitors, reducing the ability of beta-adrenergic receptors to produce cAMP in sufficient amount to maintain bronchial tone. ,
Future studies with larger sample, addition of provocative tests for diagnosis of OA and assessment of permissible amount of isocyanate in industry can be done for better results and for primordial prevention of respiratory morbidity.
| Conclusion|| |
On the basis of history taking and clinical findings, we conclude that the lung functions will decline with increasing duration (>5 years) of isocyanate exposure. Based on the above findings we recommend the following.
The worker should wear mask during painting.
Pre-employment medical examination: PFTs and X-ray chest should be done once in a year after 1 year of exposure.
Regular use of all preventive measures like face mask, Splash gloves, barrier cream, etc.
Avoidance of smoking, tobacco, regular exercise, lifestyle modification.
It is well known that the cessation of occupational exposure to a sensitizing agent may modify airway caliber or bronchial reactivity.
| Acknowledgment|| |
My sincere thanks to Dr. Basavangowdappa Principal, Dr. A. R. Gorkal professor dept of Physiology, J.S.S Medical College Mysore, for their invaluable guidance and support for the study to carry out. I also thank all those who directly or indirectly supported for the study.
| References|| |
|1.||Chan-Yeung M, Malo JL. Aetiological agents in occupational asthma. Eur Respir J 1994;7:346-71. |
|2.||Tarlo SM, Liss GM. Diisocyanate- induced asthma: Diagnosis, prognosis and effects of medical surveillance measures. Appl Occup Environ Hyg 2002;17:902-8. |
|3.||National Institute of Occupational Safety and Health. Safety and health in automobile repair shops. Cincinnati: US Department of Health and Human Services; 1977. |
|4.||Banks DE, Butcher BT, Salvaggio JE. Isocyanate induced respiratory disease. Ann Allergy 1986;57:389-97. |
|5.||Occupational Health Clinics for Ontario Workers Inc.org Isocyanates in autobody repair. Available from: http://www.ohcow.on.ca. [Last Revised on 2005, Accessed on 2010Sep(04). |
|6.||Fuchs S, Valade P. Clinical and experimental sequelae in diisocyanate exposed professionales. Arch Mal Prof 1951;12:191-6. |
|7.||Bernstein JA. Isocyanate induced pulmonary disease. J Allergy Clin Immunol 1982;70:24-31. |
|8.||Scheel LD, Killens R, Josephson A. Immunochemical aspects of TDI toxicity. Am Ind Hyg Assoc J 1964;2:179-84. |
|9.||Beckett WS. Occupational respiratory diseases. N Engl J Med 2000;342:406-13. |
|10.||Parker DL, Himrich B, Anita M, Waller KA. Cross sectional study of pulmonary function in autobody repair workers. Am J Public Health 1991;81:768-71. |
|11.||Eifan AO, Derman O, Kanbar N, Sekerel BE, Kutluk T. Occupational asthma in apprentice adolescent car painters. Pediatr Allergy Immunol 2005;16:662-8. |
|12.||American Thoracic Society. Lung function testing: Selection of reference values and interpretative stratergies. Am Rev Respir Dis 1991;144:1202-18. |
|13.||Townsend MC. ACOEM position statement spirometry in the occupational setting.American College of Occupational and Environmental Medicine. J Occup Environ Med 2000;3:228-45. |
|14.||U S Department of Defense. Occupational Medical surveillance Manual.May 1998. Publication No. DOD 6055.5-M. Available from: http://www.osha-slc.gov/SLTC/medicalsurveillanc [Last accessed on 2007 Sep 04]. |
|15.||U S Department of Health and Human Services, Public Health Services Centre for Disease Control, National Institute of Occupational Safety and Health. J NIOSH Criteria Documents Plus1997;97:502-82. |
|16.||American Thoracic Society. Evaluation of impairment/disability secondary to respiratory disorders. Am Rev Respir Dis 1986;133:1205-9. |
|17.||Schwarz DA, Baker EL. Respiratory illness in the construction industry. Airflow obstruction among painters. Chest 1988;93;134-7. |
|18.||Khanzadeh A, Rivas F. Exposure to isocyanate and organicsolvents and changes in workers in polyurethane molding process. J Occup Environ Med 1996;38;1205-12. |
|19.||Chattopadhyay O. Pulmonary function in automobile repair workers. Ind J Comm Med 2007;32:1. |
|20.||Diem JE, Jones RN, Hendrik DJ, Glindmeyer HW, Dharmarajan V, Butcher BT, et al. Five years longitudinal study of workers employed in a new toluene di-isocynate manufacturing plant. Am Rev Respir Dis 1982;126:420-8. |
|21.||Sparer J, Stowe MH, Bello D, Youngs F, Cullen MR, Liu Y, et al. Isocyanate exposure inautobody Shopworkers-TheSpray study. J Occup Environ Hyg 2004;1:570-81. |
|22.||Mapp CE, Boschetto P, Dal-vecchio L, Fabri LM. Occupational asthma due to isocyanate. Eur Respir J 1988;1:273-9. |
|23.||Torling G, Alexandersson R, Hedenstierna G, Plato N. Decreased lung function and exposure to diisocyanatein carPainters. Observations on re-examination 6yr after Initial study. Am J Ind Med 1990;17:299-310. |
|24.||Ucgun I, Ozdemir N, Metintas M, Kolsuz L. Prevalence of occupational asthma among automobile and furniture painters in the centre of Turkey. The effects of atopy andsmoking habits in occupational asthma. Allergy 1998;53:1096-100. |
|25.||Hammond SK, Gold E, Baker R, Smith W, Quinlan P, Balmes J, et al. Respiratory health effects related to occupational spray painting and welding. J Occup Environ Med 2005;47;728-39. |
|26.||Dahlqvist M, Tornling G, Plato N, Ulfvarson U. Effects within weekon FVC arecorrelated with longterm changes in pulmonary functions: Reanalysis of studies on carpainters exposed to isocyanate. Occup Environ Med 1995;53:192-5. |
|27.||Gee JB, Morgan WK. A10yr follow up study of a group of workers exposed to Isocyanate. J Occup Med 1985;34:263-71. |
|28.||Karol MH, Sandberg T, Riley EJ. Longitudinal study of tolyl reactive IgEantibodies in workershypersensitive to TDI. J Occup Med 1979;21:354-8. |
|29.||Davies RJ, Butcher BT, O′Neil CE, Salvaggio JE. The in vitro effect of TDI onlymphocyte cAMP production by isoproterenol, prostaglandin and histamine: A possible mode of action. J Allergy Clin Immunol 1977;60:223-9. |
[Figure 1], [Figure 2]
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7]