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Chronic cough due to occupational factors

Journal of Occupational Medicine and Toxicology volume 1, Article number: 3 (2006) Cite this article

Abstract

Within the large variety of subtypes of chronic cough, either defined by their clinical or pathogenetic causes, occupational chronic cough may be regarded as one of the most preventable forms of the disease. Next to obstructive airway diseases such as asthma or chronic obstructive pulmonary disease, which are sometimes concomitant with chronic cough, this chronic airway disease gains importance in the field of occupational medicine since classic fiber-related occupational airway diseases will decrease in the future.

Apart from acute accidents and incidental exposures which may lead to an acute form of cough, there are numerous sources for the development of chronic cough within the workplace. Over the last years, a large number of studies has focused on occupational causes of respiratory diseases and it has emerged that chronic cough is one of the most prevalent work-related airway diseases. Best-known examples of occupations related to the development of cough are coal miners, hard-rock miners, tunnel workers, or concrete manufacturing workers.

As chronic cough is often based on a variety of non-occupational factors such as tobacco smoke, a distinct separation into either occupational or personally -evoked can be difficult. However, revealing the occupational contribution to chronic cough and to the symptom cough in general, which is the commonest cause for the consultation of a physician, can significantly lead to a reduction of the socioeconomic burden of the disease.

Introduction

Not only since its association to exposed firefighters after the collapse of the World Trade Center [1] or work-related stress [2] is chronic cough discussed as a potential work-related disease. Chronic cough is a common disease [3] and the entity occupation-related chronic cough could be defined as a disease state that is characterized bythe presence of cough for a period longer than three months per year which is caused by an occupational exposure to an airway irritant. A cessation of the symptoms should be observed when the occupational exposure is discontinued.

Pathophysiologically, the disease is most probably dependant on the activation of two different types of sensory receptors in the respiratory innervation: C-fibre receptors with non-myelinated afferent nerve fibres, and rapidly adapting receptors (RARs) which are localized to thin myelinated A. fibres [4, 5]. Also, an increased expression of transient receptor potential vanilloid-1 has been recently demonstrated in airway nerves of patients with chronic cough [6, 7] and airway nerves and their mediators in general are likely to play an important role in the pathology of cough and airway inflammation [8–11].

It has recently been shown that COPD and to a lesser extent also asthma and rhinitis are associated with a substantially shortened work life [12]. Workplace-related chronic cough may often be found concomitant with obstructive respiratory diseases such as occupational asthma or chronic obstructive bronchitis (COPD) and in general with work-related airflow limitation which occurs due to an exposure to allergens, toxins or organic dusts such asflax, sisal, cotton (byssinosis), or hemp.

In contrast to the current knowledge on the pathophysiology and epidemiology of occupational asthma, rhinitis or COPD, which were assessed by numerous experimental [13–16] and clinical [17–21] studies, workplace-related chronic cough has never been directly focused by epidemiological or experimental studies. However, due to the simple definition and the high prevalence, cough symptoms were included to many questionnaires on occupational asthma and COPD and therefore, reviewing the literature also reveals a major role of cough as a work-related disease.

Evidence for an occupational contribution to Chronic Cough

Animal studies

In contrast to the large number of studies and animal models on asthma and COPD [22–26], there are only a few reports on animal models of cough. Therefore, a clearly established experimental link only exists for occupational causes of asthma and COPD, including allergens, irritants such as TDI [27] or other noxious gases such as NO2 [28], SO2 [29] or ozone [30, 31], Due to the need for a suitable model which offers the closest proximity to the human condition [32], ongoing research still aims to establish a model which can then be examined for the influence of occupational triggers of cough. Existing animal models of cough include guinea pigs [33, 34], rats and mice [35] but within each of these species, significant limitations concerning the neurophysiology of the cough reflex have been found [32]. In contrast to epidemiological studies for the relation between workplace exposure and respiratory symptoms in workers, which always include cough as symptom, the large number of studies on the respiratory effects of occupational noxious substances such as silica or vanadium in animals [36, 37] did not include a cough assessment due to methodological difficulties.

Epidemiologic studies

It is generally accepted that active of passive exposure to tobacco smoke can be a factor leading not only to COPD but also to cough. Due to the still large prevalence of active and passive exposure to smoke, it is difficult to isolate the effects of occupational exposures on the development and progression of cough.

However, there is increasing evidence present that demonstrates the involvement of specific occupational substances in the development of chronic cough. In this respect, a number of studies have addressed the associations between the disease and different occupational exposures:

Exposure in mines

A variety of studies has examined the relation between occupational exposure in mines and chronic cough. In a study including 970 coal-miners without pneumoconiosis, chronic cough was found in 50.5% of a group of. In 14.7% of these individuals the cough was not connected to chronic phlegm. It was therefore concluded that this subtype of non productive chronic cough displays a common disease within coal miners and that it may not be neglected in the natural history of chronic bronchitis in coal-miners. The changes in lung function were reported to be similar in non-productive and productive chronic cough [38].

The relation between chronic cough, coal mining and coal miners' pneumoconiosis (CMP) was examined in 205 miners with simple CWP and 289 without CWP, as a coincidence of pneumoconiosis and chronic cough was suggested before but had never been proofed. Logistic regression and multiple linear regression analysis were used to assess the independent effect of CWP and the miners with CWP had higher prevalences of respiratory symptoms. Also, after the adjustment for smoking, age, and years of underground mining work, CWP was associated with an increased risk and it was thus concluded that the simple coal miners' pneumoconiosis is a contributor to a significantly increased risk to develop chronic cough [39].

A further study on 242 Utah underground coal miners (mean age: 56 years) who had spent a mean of 29 years in the coal-mining industry revealed that exposure to coal mine dust had a significant influence in causing the symptom complex of chronic cough and sputum production, and coal worker's pneumoconiosis. There was a significant association among nonsmoking subjects between an increasing exposure to the coal dust and coal worker's pneumoconiosis, but not for changes in the pulmonary function [40]. A later prospective study assessed whether the presence of chronic cough and chronic phlegm predicts 5-year cigarette smoking cessation in cohort of 1.118 US male coal miners. It was shown that the presence of chronic cough and phlegm initially was inversely associated with cigarette smoking cessation. However, lung function (FVC and FEV1) impairment was positively associated with cigarette smoking cessation but did not reach statistical significance [41]. In another study, the combined effects of exposure to gold mining dust with a high content of free silica and the role of tobacco smoking were examined among 2209 South African gold miners and 483 nonminers and it was shown that tobacco smoke strongly potentates the effect of the dusts [42].

A recent study provided further detailed information on the relation between chronic cough and coal mining and discriminated between exposure to silica, asbestos, and coal dusts [43]. In total, 220 workers exposed to silica, 277 workers exposed to asbestos, and 511 workers exposed to coal from three different industries in China were examined and significantly higher prevalence of chronic cough was found in workers with pneumoconiosis than those without, irrespective of dust type. Workers with stages II and III silicosis had increased rates for chronic cough and worse pulmonary function when compared to workers with equivalent coal workers' pneumoconiosis or asbestosis [43].

Chronic cough and phlegm and their relation to surface and underground mining were also examined in a cross sectional survey of 1363 Australian men [44]. Overall, the prevalence was 14%. Smoking and age exerted strong effects on the development of symptoms and after control of confounding by these two factors, it was estimated that compared with a lifetime non-miner, the odds ratio (OR) of chronic cough and phlegm was 1.8 (95% confidence interval, 1.0–3.3) for one to nine years underground mining gold, 2.5 (1.2–5.2) for 10–19 years, and 5.1 (2.4–10.9) for more than 20 years. Whereas surface mining had only small empirical effects (OR = 1.3; 95% CI, 0.6–2.5), underground mining of other minerals than gold was also associated with chronic cough and phlegm (OR = 5.1; 95% CI, 1.1–25.0) In summary it was estimated that the proportion of cases of chronic cough and phlegm in working underground miners due to occupational factors is about 50% [44].

Cement

Dust arising from cement production contains various substances and before its abolishment, asbestos was regarded as the major factor leading to occupational diseases in the cement industry [45–47]. However, dusts contain crystalline silica which is also generated in granite, glass, and mining industries and which may lead to chronic cough [48, 49] and significant associations between exposure to concrete dust and decreased lung function (FEV(1)/FVC ratio, MMEF) have been reported in concrete workers, independent of smoking habits and of a history of allergy [50] and chronic cough was also among the major health problems in other cement worker studies [51]. For instance, a cross-sectional survey of 348 Portland cement workers in Jordan [52] revealed that chronic cough was the most prevalent respiratory problem (prevalence of 18.7%) while overall pulmonary function indices were reported to be normal. As with other studies, the rate of cough increased proportionally to the number of cigarettes smoked per day. In this study, it was concluded that the inhalation of cement dust irritates the respiratory tree and causes chronic cough without markedly affecting lung function, while smoking aggravates this effect [52].

As the seriousness of pulmonary effects has not been consistently associated with the degree of exposure to cement dust and the regular use of appropriate personal protective equipment, is still not always adequately used, a study explored the prevalence of chronic cough and other respiratory symptoms such as chronic phlegm among Portland cement workers. In comparison to non-exposed individuals, a higher percentage of the cement-exposed workers reported chronic cough (30% vs. 10 %). Also, respiratory functions such as VC, FVC, FEV(1), FEV(1)/FVC, FEV(1)/VC were significantly lower in the exposed workers if compared to the unexposed workers. These differences were not explained by age, or smoked pack-years and it was concluded that adverse respiratory health effects such as chronic cough were most likely caused by the exposure to cement dust [53]. These findings are supported by further studies on the relationship between occupational Portland cement dust exposure and respiratory health which reported a higher prevalence of chronic respiratory symptoms such as chronic cough in exposed than in control workers [54].

Exposure to cement dusts is even a larger problem in non-industrialized countries as personal protection equipment is limited [55]. A study in Nigerian cement workers revealed an increased prevalence of chronic cough due to cement dust exposure (dust level in the cement depot was 30.81 mg/m3) in 52 randomly selected, directly exposed cement workers and 24 maintenance workers if compared to a control group. The exposure also lead to a significantly decreased (P less than 0.001) lung function. Furthermore, the quantity of exposure was examined and the more directly exposed cement packers had significantly (P less than 0.05) lower lung function values than less exposed cement loaders [55].

A study in three different sections of cement, yarn, and cigarette factories among 211 nonsmoking male and female workers (21–57 years) vs. 211 healthy nonsmoking and non-exposed male and female subjects (20–57 years) revealed that 24.7% of the dust-exposed subjects developed chronic cough (vs. control 9.0%). The effects of exposure to cement dusts and cotton on the respiratory health of the exposed subjects were relatively more significant (p < 0.001) than that of exposure to tobacco dust (p < 0.05) [56].

To summon up this data on chronic cough and mining, a recent study was conducted in the United States [57]. The long-term health outcomes associated with rapid declines in FEV1 observedamong some underground coal miners was determined by evaluating respiratory symptoms including chronic cough and mortality among a group of miners who had earlierdemonstrated accelerated losses of FEV1 in the U.S. National Studyof Coal Workers' Pneumoconiosis (NSCWP). The comparison with amatched referent group of miners with relatively stable lung function revealed that there was a greater incidence of chronic cough in the miners' group, indicating an increased risk for dust-exposed workers with rapid declines in FEV1 to develop chronic cough and other respiratory symptoms [57].

Construction workers

Underground and surface construction work has also been reported to be associated with the development of chronic cough. For example, underground construction work is associated to various exposures. Next to oil mist, major exposures include dust, alpha-quartz, and nitrogen dioxide [58, 59]. To examine whether underground construction workers exposed to tunneling pollutants have an increased risk of chronic cough and other respiratory symptoms, a group of workers were examined over a follow up period of 8 years and compared to other heavy construction workers. Exposure measurements were carried out to estimate personal cumulative exposure to total dust, respirable dust, alpha-quartz, oil mist, and nitrogen dioxide and it was shown that compared with the reference group the odds ratio for the occurrence of new respiratory symptoms during the follow up period was increased in the tunnel workers [60]. Compared with the reference group, and after adjustment for age and current smoking, the odds ratios for new chronic cough (morning cough or cough during the day) were increased in the tunnel workers. Respiratory symptomswere associated with cumulative exposure to respirable dust, but not with alpha-quartz.

Oil mist has been the focus of two other studies which also demonstrated that this exposure is associated to an increase in chronic cough: In a study at a large French car-making plant, subjects exposed to straight cutting oils had a significantly higher prevalence of chronic cough and/or phlegm than the control (25.7% vs. 16.3%, p = 0.048). The prevalence of cough and/or phlegm was also significantly increased with increasing duration of exposure to straight cutting oils after adjustment on smoking categories [61]. These data were confirmed in a later study, which demonstrated that the prevalence of chronic cough or phlegm was increased greater among oil mist-exposed workers than among controls (odds ratio (OR) 4.64, P = 0.002) [62].

To define the relation between commonly used brick stones and chronic cough, 233 male workers employed in two brick-manufacturing plants (mean duration of employment: 16 years) were examined and compared to 149 matched control workers. There was a significantly higher prevalence of chronic cough () in exposed workers, compared with control workers (31.8% vs. 20.1%, P < 0.05) and the increased frequency was also documented among nonsmokers studied by age and by length of employment, suggesting a work-related effect [63].

In order to relate sewage work to the development of chronic cough and other respiratory diseases, a group of 74 sewage workers were studied by their work stations (closed channels, drainage, other places) and the prevalence of chronic cough was increased in closed channel and drainage workers if compared to controls (range: 41.9–46.2% vs. 14.3%) [64].

Farming and food industry

The farming and food industry displays a further field of economy in which an increased prevalence of chronic cough may be anticipated, as there are numerous irritant substances arising from the farming and food processing [65].

A series of reports has focused on the association of chronic cough and farming. In this respect, a study was conducted among dairy farmers (n = 265) and a control group of non-exposed subjects (n = 149) to determine whether dairy farming is associated with respiratory symptoms [66]. It was shown that while the prevalence for asthma did not differ significantly, there was strong association to chronic cough, phlegm, and chronic bronchitis. It was also suggested that the combined effect of farming and smoking was synergistic on chronic cough [66]. A larger study which did not discriminate between different farming forms confirmed these findings and reported a prevalence of 24.8 % vs. 11.4 % control) for chronic cough in farm workers [67].

To study the prevalence of chronic cough and other chronic and acute respiratory symptoms in livestock farm workers raising cattle and horses, a cross-sectional study and lung function tests were performed in 236 (169 male and 67 female) subjects [68]. The study demonstrated that there was a significantly higher prevalence of almost all chronic respiratory symptoms in farmers, and the highest prevalence was found for chronic cough in men (27.2%). As with many other studies, a logistic regression analysis indicated significant effects of smoking (P < 0.001). In this study, a large number of male and female livestock farm workers also complained of acute dry cough (52.2%) at the place of work [68].

In contrast to cattle farmers, swine confinement farms are differently exposed. To define in detail the nature and disease determinants in this exposed group, a 5 year prospective study was conducted [69], and it was found that nearly 20% of swine confinement workers reported chronic cough, which was significantly more prevalent compared to a blue collar comparison group. As in livestock farms, acute work place-related cough was much more frequent than chronic cough (87% of confinement workers reported work place-related cough) [69]. Similar findings for chronic cough were also reported by a smaller study [70] and it was also shown for veterinarians, that working more than 20 hr per week in swine confinement buildings increased the odds of occurrence of chronic cough approximately three times [71].

Poultry farming has also been associated with the development of airway diseases and therefore, a group of 343 poultry farmers was studied for the prevalence of acute and chronic respiratory symptoms and lung function changes. Amongst others, there was significantly higher prevalence of chronic cough in the poultry farmers and workers exposed for more than 10 years had significantly higher symptoms prevalences than farmers with shorter exposures (except among female smokers) [72]. An additional study on a group of 57 female workers employed in the processing of poultry food and 51 non-exposed control workers showed similar results with the highest prevalence for chronic cough (49.1%), followed by dyspnea (43.9%), rhinitis (38.6%) [73].

A further report examined the respiratory health of Californian rice farmers who are occupationally exposed to various agents such as inorganic dusts and smoke from burning of agricultural waste [74]. Here, chronic cough was reported by 7.1% and was associated with reported hours per year burning rice stubble, while the prevalence for other diseases were 6.3% for chronic bronchitis and 7.1% for physician-diagnosed asthma, indicating prevalences among rice farmers [74]. A high prevalence for chronic cough was also reported for cash grain farmers in Ohio with an overall design-adjusted prevalence corresponding 95% confidence intervals (CIs) of 9.4% (CI: 7.6–11.1%) [75].

As hemp workers with a long exposure to dust were reported to develop chronic respiratory symptoms including cough, a 7 years of follow-up study was performed. Among the hemp workers, a significantly higher occurrence of chronic cough was found which was concomitant with a significantly larger annual decline of forced expiratory volume in 1 second (FEV1.0) [76]. Similarly, a study was conducted in workers exposed to flour dust in a flour mill. Here, 26.0% of the exposed subjects presented with chronic cough, indicating a strong association between exposure to flour dusts and the prevalence of chronic cough [77]. Flour dusts are also associated with a large number of occupational diseases among bakers. Parallel to the findings in flour mill workers, it was shown that in bakers a greater prevalence of chronic cough and sputum can be found [78].

The influence of grain processing on the prevalence of respiratory diseases was also studied in dock workers who load grain cargoes and dock workers who work in grain elevators. It was found that the prevalences of chronic cough were similar in both group and the risks to develop symptoms were significantly increased for the dock workers if compared to non-exposed workers from the same regions [79].

Next to flour mill workers and grain workers, workers in other food-producing facilities have also been reported to have increased prevalences of chronic cough. In this respect chronic cough was found in potato-processing workers [80] and in spice factory workers [81]. But also, workers who are not as highly exposed to dusts have been reported to develop chronic cough. For instance, vegetable pickers [82] or greenhouse workers [83] were reported to have higher prevalences of chronic cough and also workers who process mushrooms [84–86].

Wood industry

Whereas exposure to wood dusts is known for occupational diseases such as cancer [87–89], chronic cough has also long been discussed as wood-dust related [90]. For instance, a study on respiratory symptoms in differentially exposed pine sawmill workers revealed adjusted odds ratios for cough at 2.7 (1.2–6.5) for the low, 5.2 (2.1–13.0) for the high 'green dust' and 3.3 (1.4–7.9) for the high 'dry dust' exposure groups. It was concluded that working in pine sawmills is associated with an increased prevalence of cough, next to eye and nose irritation and asthma [91]. Wood dust exposure was also the focus of a study among furniture workers and it was shown that dry cough was the most common illness [92]. Similarly, in a paper mill cohort consisting of workers with high cumulative exposure (n = 313), with medium cumulative exposure (n = 321), and with low cumulative exposure (n = 338) to paper dust, elevated prevalence ratios for chronic cough and chronic phlegm were found after adjustment for smoking and gender [93]. Also, paper recycling is associated with an increased risk for chronic cough, which had the highest prevalence (36.6%) of all respiratory symptoms [94].

Chemicals

Next to associations between chronic cough and farming or wood dusts, cough may also arise from chronic irritation of respiratory nerves by chemicals and various studies have addressed this question.

For exposure to methylmethacrylate (MMA) it was shown that 20% of subject in the MMA-exposed group had chronic cough compared with 1% in the control [95]. Also, a study among workers of a polyvinylchloride (PVC) factory suggested chronic cough and chronic phlegm may be developed due to exposure to vinyl chloride monomer, PVC dust, PVC thermal degradation products and other non-identified substances [96]. A smaller study among workers who were exposed to aliphatic polyamines in a chemical factory gave further evidence to a relation between exposure to chemicals and chronic cough [97] and a need for stringent measures to protect the respiratory health of industrial workers exposed to aliphatic amines was proposed [97].

Dental technicians are exposed to a large variety of chemicals and as with furriers, these occupations were reported to be associated to chronic cough [98, 99].

Next to these exposure in the chemical industry, a variety of other substances including latex [100] was reported to be related to chronic cough and also the surrounding of the work place, i.e., cold houses, may contribute to the prevalence of cough [101].

General studies

Next to the large amount of studies which focused on a specific occupational background, there are several studies which were conducted in random samples and examined for relationships between occupational exposure chronic respiratory symptoms.

Data analysis from a random sample of 8,515 adults from 6 cities in the eastern and Midwestern United States [102] revealed that 31% of the population was occupationally exposed to dust and 30% of the population was exposed to gas or fumes. After adjusting for smoking habits, gender, age, and city of residence, subjects with either occupational exposure had significantly elevated prevalences of chronic cough. In summary, the data demonstrated that chronic respiratory symptoms and disease can be independently associated with occupational exposures [102].

A longitudinal analysis of the relationship between incidence rates of chronic respiratory symptoms over 13 years and occupational exposure during the first five years of follow-up in 1132 males and 1598 females (19 to 60 years of age) in Cracow, Poland [103] came to similar results [103] and confirmed the results of cross-sectional studies which have indicated deleterious effects of even moderate occupational exposures on respiratory symptoms [103].

Other studies in France [104] Spain [105] confirmed these data. In an un-polluted rural area of North Italy, the effects of occupational exposure in a general population sample (age range of 18 to 64 yr) with 417 participants who reported any exposure to dusts, chemicals, or gases and 1,218 who reported no exposure were examined. In summary, multiple logistic models in the overall group, accounting for age, smoking, and pack-years, demonstrated that self-reported occupational exposure was associated significantly with higher risks for cough (odds ratio: 1.69), suggesting a causal association between occupational exposure and chronic pulmonary diseases such as cough [106].

A recent statement of the American Thoracic Society addressed the occupational contribution to the burden of airway disease [107]. This statement reviewed the evidence implicating occupational factors in the pathogenesis of the obstructive airway diseases asthma and COPD and tried to quantifythe contribution of the work-related risks to the burden of thesediseases in the general population.

The quantification was performed using an assessment of the population attributable risk (PAR), which is defined as the fraction of cases in a population that arise because ofcertain exposures. By analyzing the data presented on COPD, it can be seen that the disease definition is often based on chronic cough (3 + months of the year) and therefore, some of these studies have indirectly addressed chronic cough. The data of these studies on chronic cough is given in table 1. As the definition of COPD and exposure variedamong the studies analyzed, and there were less studies providing data for an estimate of the PAR of COPD due to occupation than for asthma, there was a greateruncertainty about the estimate but nonetheless, a valueof 15% was reported to be a reasonable estimate of the occupational contributionto the population burden of COPD [107].

Table 1 Chronic cough: population-attributable risk due to occupation. Table modified from 107. Abbreviations: ECRHS = European Community Respiratory Health Survey; PAARC = Pollution Atmosphérique et Affections Respiratoires Chroniques/Air Pollution and Respiratory Diseases; PAR% = magnitude of the population attributable risk.
Full size table

Conclusion

There is a large amount of epidemiological data pointing to an association between occupational exposure and the prevalence of chronic cough.

However, as chronic cough is often based on a variety of non-occupational but factors such as exposure to tobacco smoke, a distinct separation into either occupational or personally -associated can be difficult. Future experimental and epidemiological studies can lead to a better understanding of the occupational hazards which may cause chronic cough and establish a stronger link between the entity of chronic cough and specific occupations. Therefore, next to enlarging the epidemiological knowledge on the occupational contribution to the disease [108], experimental studies encompassing modern techniques from molecular biology [109, 110], physiology [111–113] and morphology [114–116] should be used to identify a cellular basis of work-related chronic cough.

References

  1. Prezant DJ, Weiden M, Banauch GI, McGuinness G, Rom WN, Aldrich TK, Kelly KJ: Cough and bronchial responsiveness in firefighters at the World Trade Center site. N Engl J Med 2002, 347: 806–815. 10.1056/NEJMoa021300

    PubMed  Google Scholar 

  2. Cheng Y, Guo YL, Yeh WY: A national survey of psychosocial job stressors and their implications for health among working people in Taiwan. Int Arch Occup Environ Health 2001, 74: 495–504. 10.1007/s004200100254

    CAS  PubMed  Google Scholar 

  3. Currie GP, Gray RD, McKay J: Chronic cough. Bmj 2003, 326: 261. 10.1136/bmj.326.7383.261

    PubMed Central  PubMed  Google Scholar 

  4. Groneberg DA, Quarcoo D, Frossard N, Fischer A: Neurogenic mechanisms in bronchial inflammatory diseases. Allergy 2004, 59: 1139–1152. 10.1111/j.1398-9995.2004.00665.x

    CAS  PubMed  Google Scholar 

  5. Stone R: Chronic cough--mechanisms and management. Respir Med 1993, 87: 249–251. 10.1016/0954-6111(93)90020-Z

    CAS  PubMed  Google Scholar 

  6. Groneberg DA, Niimi A, Dinh QT, Cosio B, Hew M, Fischer A, Chung KF: Increased expression of transient receptor potential vanilloid-1 in airway nerves of chronic cough. Am J Respir Crit Care Med 2004, 170: 1276–1280. 10.1164/rccm.200402-174OC

    PubMed  Google Scholar 

  7. Trevisani M, Gazzieri D, Benvenuti F, Campi B, Dinh QT, Groneberg DA, Rigoni M, Emonds-Alt X, Creminon C, Fischer A, Geppetti P, Harrison S: Ethanol Causes Inflammation in the Airways by a Neurogenic and TRPV1-Dependent Mechanism. J Pharmacol Exp Ther 2004.

    Google Scholar 

  8. Springer J, Amadesi S, Trevisani M, Harrison S, Dinh QT, McGregor GP, Fischer A, Geppetti P, Groneberg DA: Effects of alpha calcitonin gene-related peptide in human bronchial smooth muscle and pulmonary artery. Regul Pept 2004, 118: 127–134. 10.1016/j.regpep.2003.11.006

    CAS  PubMed  Google Scholar 

  9. Fischer A, Wussow A, Cryer A, Schmeck B, Noga O, Zweng M, Peiser C, Dinh QT, Heppt W, Groneberg DA: Neuronal plasticity in persistent perennial allergic rhinitis. J Occup Environ Med 2005, 47: 20–25.

    CAS  PubMed  Google Scholar 

  10. Thai Dinh Q, Groneberg DA, Peiser C, Joachim RA, Frossard N, Arck PC, Klapp BF, Fischer A: Expression of substance P and nitric oxide synthase in vagal sensory neurons innervating the mouse airways. Regul Pept 2005, 126: 189–194. 10.1016/j.regpep.2004.09.006

    PubMed  Google Scholar 

  11. Springer J, Groneberg DA, Pregla R, Fischer A: Inflammatory cells as source of tachykinin-induced mucus secretion in chronic bronchitis. Regul Pept 2005, 124: 195–201. 10.1016/j.regpep.2004.07.017

    CAS  PubMed  Google Scholar 

  12. Yelin E, Katz P, Balmes J, Trupin L, Earnest G, Eisner M, Blanc P: Work Life of Persons with Asthma, Rhinitis, and COPD: A Study Using a National, Population-Based Sample. J Occup Med Toxicol 2005, 1: 2. 10.1186/1745-6673-1-2

    Google Scholar 

  13. Groneberg DA, Heppt W, Welker P, Peiser C, Dinh QT, Cryer A, Zweng M, Witt C, Fischer A: Aspirin-sensitive rhinitis associated changes in upper airway innervation. Eur Respir J 2003, Im Druck.

    Google Scholar 

  14. Heppt W, Thai Dinh Q, Cryer A, Zweng M, Noga O, Peiser C, Melvan M, Witt C, Fischer A, Groneberg DA: Phenotypic alteration of neuropeptide-containing nerve fibres in seasonal intermittent allergic rhinitis. Clin Exp Allergy 2004, 34: 1105–1110. 10.1111/j.1365-2222.2004.01990.x

    CAS  PubMed  Google Scholar 

  15. Groneberg DA, Heppt W, Cryer A, Wussow A, Peiser C, Zweng M, Dinh QT, Witt C, Fischer A: Toxic rhinitis-induced changes of human nasal mucosa innervation. Toxicol Pathol 2003, 31: 326–331. 10.1080/01926230309749

    CAS  PubMed  Google Scholar 

  16. Heppt W, Peiser C, Cryer A, Dinh QT, Zweng M, Witt C, Fischer A, Groneberg DA: Innervation of human nasal mucosa in environmentally triggered hyperreflectoric rhinitis. J Occup Environ Med 2002, 44: 924–929.

    CAS  PubMed  Google Scholar 

  17. Arnaiz NO, Kaufman JD: New developments in work-related asthma. Clin Chest Med 2002, 23: 737–747. 10.1016/S0272-5231(02)00034-5

    PubMed  Google Scholar 

  18. Zacharisen MC: Occupational asthma. Med Clin North Am 2002, 86: 951–971. 10.1016/S0025-7125(02)00030-5

    CAS  PubMed  Google Scholar 

  19. Siracusa A, Marabini A, Pace ML: Occupational rhinitis. Monaldi Arch Chest Dis 2002, 57: 127–129.

    CAS  PubMed  Google Scholar 

  20. Balmes JR: Occupational airways diseases from chronic low-level exposures to irritants. Clin Chest Med 2002, 23: 727–35, vi. 10.1016/S0272-5231(02)00031-X

    PubMed  Google Scholar 

  21. Viegi G, Di Pede C: Chronic obstructive lung diseases and occupational exposure. Curr Opin Allergy Clin Immunol 2002, 2: 115–121. 10.1097/00130832-200204000-00006

    PubMed  Google Scholar 

  22. Chung KF, Caramori G, Groneberg DA: Airway obstruction in chronic obstructive pulmonary disease. N Engl J Med 2004, 351: 1459–1461. 10.1056/NEJM200409303511420

    CAS  PubMed  Google Scholar 

  23. Castranov V, Frazer DG, Manley LK, Dey RD: Pulmonary alterations associated with inhalation of occupational and environmental irritants. Int Immunopharmacol 2002, 2: 163–172. 10.1016/S1567-5769(01)00169-2

    Google Scholar 

  24. Groneberg DA, Chung KF: Models of chronic obstructive pulmonary disease. Respir Res 2004, 5: 18. 10.1186/1465-9921-5-18

    PubMed Central  PubMed  Google Scholar 

  25. Kerzel S, Path G, Nockher WA, Quarcoo D, Raap U, Groneberg DA, Dinh QT, Fischer A, Braun A, Renz H: Pan-neurotrophin receptor p75 contributes to neuronal hyperreactivity and airway inflammation in a murine model of experimental asthma. Am J Respir Cell Mol Biol 2003, 28: 170–178. 10.1165/rcmb.4811

    CAS  PubMed  Google Scholar 

  26. Chung KF, Groneberg DA: Effects of cigarette smoke on pulmonary homeostasis. Am J Respir Cell Mol Biol 2005, 32: 167. 10.1165/rcmb.F288

    CAS  PubMed  Google Scholar 

  27. Pons F, Haag M, Corcos L, Bonnet P, Guillouzo A, Lugnier A, Frossard N: Inhalation of toluene diisocyanate affects cytochrome P450 2B1 expression in rat lung. Arch Toxicol 2000, 74: 397–403. 10.1007/s002040000153

    CAS  PubMed  Google Scholar 

  28. Barth PJ, Uhlarik S, Bittinger A, Wagner U, Ruschoff J: Diffuse alveolar damage in the rat lung after short and long term exposure to nitrogen dioxide. Pathol Res Pract 1994, 190: 33–41.

    CAS  PubMed  Google Scholar 

  29. Kodavanti UP, Mebane R, Ledbetter A, Krantz T, McGee J, Jackson MC, Walsh L, Hilliard H, Chen BY, Richards J, Costa DL: Variable pulmonary responses from exposure to concentrated ambient air particles in a rat model of bronchitis. Toxicol Sci 2000, 54: 441–451. 10.1093/toxsci/54.2.441

    CAS  PubMed  Google Scholar 

  30. Hisada T, Salmon M, Nasuhara Y, Chung KF: Involvement of haemoxygenase-1 in ozone-induced airway inflammation and hyperresponsiveness. Eur J Pharmacol 2000, 399: 229–234. 10.1016/S0014-2999(00)00369-1

    CAS  PubMed  Google Scholar 

  31. Harkema JR, Hotchkiss JA: Ozone- and endotoxin-induced mucous cell metaplasias in rat airway epithelium: novel animal models to study toxicant-induced epithelial transformation in airways. Toxicol Lett 1993, 68: 251–263. 10.1016/0378-4274(93)90136-L

    CAS  PubMed  Google Scholar 

  32. Belvisi MG, Bolser DC: Summary: animal models for cough. Pulm Pharmacol Ther 2002, 15: 249–250. 10.1006/pupt.2002.0349

    CAS  PubMed  Google Scholar 

  33. Fox AJ, Barnes PJ, Venkatesan P, Belvisi MG: Activation of large conductance potassium channels inhibits the afferent and efferent function of airway sensory nerves in the guinea pig. J Clin Invest 1997, 99: 513–519.

    CAS  PubMed Central  PubMed  Google Scholar 

  34. Lalloo UG, Fox AJ, Belvisi MG, Chung KF, Barnes PJ: Capsazepine inhibits cough induced by capsaicin and citric acid but not by hypertonic saline in guinea pigs. J Appl Physiol 1995, 79: 1082–1087.

    CAS  PubMed  Google Scholar 

  35. Kamei J, Iwamoto Y, Suzuki T, Misawa M, Nagase H, Kasuya Y: Antitussive effects of naltrindole, a selective delta-opioid receptor antagonist, in mice and rats. Eur J Pharmacol 1993, 249: 161–165. 10.1016/0014-2999(93)90428-K

    CAS  PubMed  Google Scholar 

  36. Bonner JC, Rice AB, Moomaw CR, Morgan DL: Airway fibrosis in rats induced by vanadium pentoxide. Am J Physiol Lung Cell Mol Physiol 2000, 278: L209–16.

    CAS  PubMed  Google Scholar 

  37. Churg A, Hobson J, Wright J: Functional and morphologic comparison of silica- and elastase-induced airflow obstruction. Exp Lung Res 1989, 15: 813–822.

    CAS  PubMed  Google Scholar 

  38. Potkonjak V: Prevalence and etiology of chronic cough without sputum production in coal miners. Rev Inst Hyg Mines (Hasselt) 1979, 34: 191–202.

    CAS  Google Scholar 

  39. Wang X, Yu IT, Wong TW, Yano E: Respiratory symptoms and pulmonary function in coal miners: looking into the effects of simple pneumoconiosis. Am J Ind Med 1999, 35: 124–131. 10.1002/(SICI)1097-0274(199902)35:2<124::AID-AJIM3>3.0.CO;2-M

    CAS  PubMed  Google Scholar 

  40. Rom WN, Kanner RE, Renzetti ADJ, Shigeoka JW, Barkman HW, Nichols M, Turner WA, Coleman M, Wright WE: Respiratory disease in Utah coal miners. Am Rev Respir Dis 1981, 123: 372–377.

    CAS  PubMed  Google Scholar 

  41. Ames RG, Hall DS: Smoking cessation among coal miners as predicted by baseline respiratory function and symptoms: a 5-year prospective study. Prev Med 1985, 14: 181–186. 10.1016/0091-7435(85)90033-7

    CAS  PubMed  Google Scholar 

  42. Hnizdo E, Baskind E, Sluis-Cremer GK: Combined effect of silica dust exposure and tobacco smoking on the prevalence of respiratory impairments among gold miners. Scand J Work Environ Health 1990, 16: 411–422.

    CAS  PubMed  Google Scholar 

  43. Wang XR, Christiani DC: Respiratory symptoms and functional status in workers exposed to silica, asbestos, and coal mine dusts. J Occup Environ Med 2000, 42: 1076–1084.

    CAS  PubMed  Google Scholar 

  44. Holman CD, Psaila-Savona P, Roberts M, McNulty JC: Determinants of chronic bronchitis and lung dysfunction in Western Australian gold miners. Br J Ind Med 1987, 44: 810–818.

    CAS  PubMed Central  PubMed  Google Scholar 

  45. Tuch H, Tulchinsky TH, Casper M, Knaane H: Medical screening of former asbestos cement workers in Israel: a pilot program. Am J Ind Med 1986, 10: 471–478.

    CAS  PubMed  Google Scholar 

  46. Mattioli S, Nini D, Mancini G, Violante FS: Past asbestos exposure levels in foundries and cement-asbestos factories. Am J Ind Med 2002, 42: 363. 10.1002/ajim.10114

    PubMed  Google Scholar 

  47. Algranti E, Mendonca EM, DeCapitani EM, Freitas JB, Silva HC, Bussacos MA: Non-malignant asbestos-related diseases in Brazilian asbestos-cement workers. Am J Ind Med 2001, 40: 240–254. 10.1002/ajim.1095

    CAS  PubMed  Google Scholar 

  48. Calvert GM, Rice FL, Boiano JM, Sheehy JW, Sanderson WT: Occupational silica exposure and risk of various diseases: an analysis using death certificates from 27 states of the United States. Occup Environ Med 2003, 60: 122–129. 10.1136/oem.60.2.122

    CAS  PubMed Central  PubMed  Google Scholar 

  49. Kalacic I: Chronic nonspecific lung disease in cement workers. Arch Environ Health 1973, 26: 78–83.

    CAS  PubMed  Google Scholar 

  50. Meijer E, Kromhout H, Heederik D: Respiratory effects of exposure to low levels of concrete dust containing crystalline silica. Am J Ind Med 2001, 40: 133–140. 10.1002/ajim.1080

    CAS  PubMed  Google Scholar 

  51. Abou-Taleb AN, Musaiger AO, Abdelmoneim RB: Health status of cement workers in the United Arab Emirates. J R Soc Health 1995, 115: 378–381.

    CAS  PubMed  Google Scholar 

  52. AbuDhaise BA, Rabi AZ, al Zwairy MA, el Hader AF, el Qaderi S: Pulmonary manifestations in cement workers in Jordan. Int J Occup Med Environ Health 1997, 10: 417–428.

    CAS  PubMed  Google Scholar 

  53. Al-Neaimi YI, Gomes J, Lloyd OL: Respiratory illnesses and ventilatory function among workers at a cement factory in a rapidly developing country. Occup Med (Lond) 2001, 51: 367–373. 10.1093/occmed/51.6.367

    CAS  Google Scholar 

  54. Yang CY, Huang CC, Chiu HF, Chiu JF, Lan SJ, Ko YC: Effects of occupational dust exposure on the respiratory health of Portland cement workers. J Toxicol Environ Health 1996, 49: 581–588. 10.1080/009841096160637

    CAS  PubMed  Google Scholar 

  55. Oleru UG: Pulmonary function and symptoms of Nigerian workers exposed to cement dust. Environ Res 1984, 33: 379–385. 10.1016/0013-9351(84)90036-7

    CAS  PubMed  Google Scholar 

  56. Mengesha YA, Bekele A: Relative chronic effects of different occupational dusts on respiratory indices and health of workers in three Ethiopian factories. Am J Ind Med 1998, 34: 373–380. 10.1002/(SICI)1097-0274(199810)34:4<373::AID-AJIM11>3.0.CO;2-#

    CAS  PubMed  Google Scholar 

  57. Beeckman LA, Wang ML, Petsonk EL, Wagner GR: Rapid declines in FEV1 and subsequent respiratory symptoms, illnesses, and mortality in coal miners in the United States. Am J Respir Crit Care Med 2001, 163: 633–639.

    CAS  PubMed  Google Scholar 

  58. Sullivan PA, Bang KM, Hearl FJ, Wagner GR: Respiratory disease risks in the construction industry. Occup Med 1995, 10: 313–334.

    CAS  PubMed  Google Scholar 

  59. Ulvestad B, Bakke B, Melbostad E, Fuglerud P, Kongerud J, Lund MB: Increased risk of obstructive pulmonary disease in tunnel workers. Thorax 2000, 55: 277–282. 10.1136/thorax.55.4.277

    CAS  PubMed Central  PubMed  Google Scholar 

  60. Ulvestad B, Bakke B, Eduard W, Kongerud J, Lund MB: Cumulative exposure to dust causes accelerated decline in lung function in tunnel workers. Occup Environ Med 2001, 58: 663–669. 10.1136/oem.58.10.663

    CAS  PubMed Central  PubMed  Google Scholar 

  61. Ameille J, Wild P, Choudat D, Ohl G, Vaucouleur JF, Chanut JC, Brochard P: Respiratory symptoms, ventilatory impairment, and bronchial reactivity in oil mist-exposed automobile workers. Am J Ind Med 1995, 27: 247–256.

    CAS  PubMed  Google Scholar 

  62. Massin N, Bohadana AB, Wild P, Goutet P, Kirstetter H, Toamain JP: Airway responsiveness, respiratory symptoms, and exposures to soluble oil mist in mechanical workers. Occup Environ Med 1996, 53: 748–752.

    CAS  PubMed Central  PubMed  Google Scholar 

  63. Zuskin E, Mustajbegovic J, Schachter EN, Kern J, Doko-Jelinic J, Godnic-Cvar J: Respiratory findings in workers employed in the brick-manufacturing industry. J Occup Environ Med 1998, 40: 814–820. 10.1097/00043764-199809000-00011

    CAS  PubMed  Google Scholar 

  64. Zuskin E, Mustajbegovic J, Schachter EN: Respiratory function in sewage workers. Am J Ind Med 1993, 23: 751–761.

    CAS  PubMed  Google Scholar 

  65. Linaker C, Smedley J: Respiratory illness in agricultural workers. Occup Med (Lond) 2002, 52: 451–459. 10.1093/occmed/52.8.451

    CAS  Google Scholar 

  66. Dalphin JC, Dubiez A, Monnet E, Gora D, Westeel V, Pernet D, Polio JC, Gibey R, Laplante JJ, Depierre A: Prevalence of asthma and respiratory symptoms in dairy farmers in the French province of the Doubs. Am J Respir Crit Care Med 1998, 158: 1493–1498.

    CAS  PubMed  Google Scholar 

  67. Kern J, Mustajbegovic J, Schachter EN, Zuskin E, Vrcic-Keglevic M, Ebling Z, Senta A: Respiratory findings in farmworkers. J Occup Environ Med 2001, 43: 905–913.

    CAS  PubMed  Google Scholar 

  68. Mustajbegovic J, Zuskin E, Schachter EN, Kern J, Vrcic-Keglevic M, Vitale K, Ebling Z: Respiratory findings in livestock farmworkers. J Occup Environ Med 2001, 43: 576–584.

    CAS  PubMed  Google Scholar 

  69. Donham KJ, Merchant JA, Lassise D, Popendorf WJ, Burmeister LF: Preventing respiratory disease in swine confinement workers: intervention through applied epidemiology, education, and consultation. Am J Ind Med 1990, 18: 241–261.

    CAS  PubMed  Google Scholar 

  70. Zhou C, Hurst TS, Cockcroft DW, Dosman JA: Increased airways responsiveness in swine farmers. Chest 1991, 99: 941–944.

    CAS  PubMed  Google Scholar 

  71. Tielen MJ, Elbers AR, Snijdelaar M, van Gulick PJ, Preller L, Blaauw PJ: Prevalence of self-reported respiratory disease symptoms among veterinarians in the Southern Netherlands. Am J Ind Med 1996, 29: 201–207. 10.1002/(SICI)1097-0274(199602)29:2<201::AID-AJIM11>3.0.CO;2-7

    CAS  PubMed  Google Scholar 

  72. Zuskin E, Mustajbegovic J, Schachter EN, Kern J, Rienzi N, Goswami S, Marom Z, Maayani S: Respiratory function in poultry workers and pharmacologic characterization of poultry dust extract. Environ Res 1995, 70: 11–19. 10.1006/enrs.1995.1040

    CAS  PubMed  Google Scholar 

  73. Zuskin E, Kanceljak B, Mustajbegovic J, Schachter EN, Stilinovic L: Respiratory symptoms and immunological status in poultry food processing workers. Int Arch Occup Environ Health 1994, 66: 339–342. 10.1007/BF00378367

    CAS  PubMed  Google Scholar 

  74. McCurdy SA, Ferguson TJ, Goldsmith DF, Parker JE, Schenker MB: Respiratory health of California rice farmers. Am J Respir Crit Care Med 1996, 153: 1553–1559.

    CAS  PubMed  Google Scholar 

  75. Wilkins JR, Engelhardt HL, Rublaitus SM, Crawford JM, Fisher JL, Bean TL: Prevalence of chronic respiratory symptoms among Ohio cash grain farmers. Am J Ind Med 1999, 35: 150–163. 10.1002/(SICI)1097-0274(199902)35:2<150::AID-AJIM7>3.0.CO;2-5

    PubMed  Google Scholar 

  76. Bouhuys A, Zuskin E: Chronic respiratory disease in hemp workers. A follow-up study, 1967–1974. Ann Intern Med 1976, 84: 398–405.

    CAS  PubMed  Google Scholar 

  77. Awad el Karim MA, Gad el Rab MO, Omer AA, el Haimi YA: Respiratory and allergic disorders in workers exposed to grain and flour dusts. Arch Environ Health 1986, 41: 297–301.

    CAS  PubMed  Google Scholar 

  78. Prichard MG, Ryan G, Musk AW: Wheat flour sensitisation and airways disease in urban bakers. Br J Ind Med 1984, 41: 450–454.

    CAS  PubMed Central  PubMed  Google Scholar 

  79. Dimich-Ward HD, Kennedy SM, Dittrick MA, DyBuncio A, Chan-Yeung M: Evaluation of the respiratory health of dock workers who load grain cargoes in British Columbia. Occup Environ Med 1995, 52: 273–278.

    CAS  PubMed Central  PubMed  Google Scholar 

  80. Milanowski J, Gora A, Skorska C, Mackiewicz B, Krysinska-Traczyk E, Cholewa G, Sitkowska J, Dutkiewicz J: The effects of exposure to organic dust on the respiratory system of potato processing workers. Ann Agric Environ Med 2002, 9: 243–247.

    PubMed  Google Scholar 

  81. Zuskin E, Skuric Z, Kanceljak B, Pokrajac D, Schachter EN, Witek TJ: Respiratory findings in spice factory workers. Arch Environ Health 1988, 43: 335–339.

    CAS  PubMed  Google Scholar 

  82. Zuskin E, Mustajbegovic J, Schachter EN, Rienzi N: Respiratory symptoms and ventilatory capacity in workers in a vegetable pickling and mustard production facility. Int Arch Occup Environ Health 1993, 64: 457–461. 10.1007/BF00517953

    CAS  PubMed  Google Scholar 

  83. Zuskin E, Schachter EN, Mustajbegovic J: Respiratory function in greenhouse workers. Int Arch Occup Environ Health 1993, 64: 521–526. 10.1007/BF00381102

    CAS  PubMed  Google Scholar 

  84. Tanaka H, Saikai T, Sugawara H, Takeya I, Tsunematsu K, Matsuura A, Abe S: Workplace-related chronic cough on a mushroom farm. Chest 2002, 122: 1080–1085. 10.1378/chest.122.3.1080

    PubMed  Google Scholar 

  85. Tanaka H, Saikai T, Sugawara H, Tsunematsu K, Takeya I, Koba H, Matsuura A, Imai K, Abe S: Three-year follow-up study of allergy in workers in a mushroom factory. Respir Med 2001, 95: 943–948. 10.1053/rmed.2001.1187

    CAS  PubMed  Google Scholar 

  86. Suzuki K, Tanaka H, Sugawara H, Saito Y, Koba H, Tsunematsu K, Abe S: Chronic hypersensitivity pneumonitis induced by Shiitake mushroom spores associated with lung cancer. Intern Med 2001, 40: 1132–1135.

    CAS  PubMed  Google Scholar 

  87. Innos K, Rahu M, Rahu K, Lang I, Leon DA: Wood dust exposure and cancer incidence: a retrospective cohort study of furniture workers in Estonia. Am J Ind Med 2000, 37: 501–511. 10.1002/(SICI)1097-0274(200005)37:5<501::AID-AJIM6>3.0.CO;2-T

    CAS  PubMed  Google Scholar 

  88. Vaughan TL, Stewart PA, Teschke K, Lynch CF, Swanson GM, Lyon JL, Berwick M: Occupational exposure to formaldehyde and wood dust and nasopharyngeal carcinoma. Occup Environ Med 2000, 57: 376–384. 10.1136/oem.57.6.376

    CAS  PubMed Central  PubMed  Google Scholar 

  89. Hildesheim A, Dosemeci M, Chan CC, Chen CJ, Cheng YJ, Hsu MM, Chen IH, Mittl BF, Sun B, Levine PH, Chen JY, Brinton LA, Yang CS: Occupational exposure to wood, formaldehyde, and solvents and risk of nasopharyngeal carcinoma. Cancer Epidemiol Biomarkers Prev 2001, 10: 1145–1153.

    CAS  PubMed  Google Scholar 

  90. Carosso A, Ruffino C, Bugiani M: Respiratory diseases in wood workers. Br J Ind Med 1987, 44: 53–56.

    CAS  PubMed Central  PubMed  Google Scholar 

  91. Douwes J, McLean D, Slater T, Pearce N: Asthma and other respiratory symptoms in New Zealand pine processing sawmill workers. Am J Ind Med 2001, 39: 608–615. 10.1002/ajim.1060

    CAS  PubMed  Google Scholar 

  92. Milanowski J, Gora A, Skorska C, Krysinska-Traczyk E, Mackiewicz B, Sitkowska J, Cholewa G, Dutkiewicz J: Work-related symptoms among furniture factory workers in Lublin region (eastern Poland). Ann Agric Environ Med 2002, 9: 99–103.

    PubMed  Google Scholar 

  93. Toren K, Jarvholm B, Sallsten G, Thiringer G: Respiratory symptoms and asthma among workers exposed to paper dust: a cohort study. Am J Ind Med 1994, 26: 489–496.

    CAS  PubMed  Google Scholar 

  94. Zuskin E, Mustajbegovic J, Schachter EN, Kanceljak B, Kern J, Macan J, Ebling Z: Respiratory function and immunological status in paper-recycling workers. J Occup Environ Med 1998, 40: 986–993. 10.1097/00043764-199811000-00009

    CAS  PubMed  Google Scholar 

  95. Marez T, Edme JL, Boulenguez C, Shirali P, Haguenoer JM: Bronchial symptoms and respiratory function in workers exposed to methylmethacrylate. Br J Ind Med 1993, 50: 894–897.

    CAS  PubMed Central  PubMed  Google Scholar 

  96. Baser ME, Tockman MS, Kennedy TP: Pulmonary function and respiratory symptoms in polyvinylchloride fabrication workers. Am Rev Respir Dis 1985, 131: 203–208.

    CAS  PubMed  Google Scholar 

  97. Ng TP, Lee HS, Malik MA, Chee CB, Cheong TH, Wang YT: Asthma in chemical workers exposed to aliphatic polyamines. Occup Med (Lond) 1995, 45: 45–48.

    CAS  Google Scholar 

  98. Radi S, Dalphin JC, Manzoni P, Pernet D, Leboube MP, Viel JF: Respiratory morbidity in a population of French dental technicians. Occup Environ Med 2002, 59: 398–404. 10.1136/oem.59.6.398

    CAS  PubMed Central  PubMed  Google Scholar 

  99. Zuskin E, Skuric Z, Kanceljak B, Pokrajac D, Schachter EN, Witek TJJ: Respiratory symptoms and lung function in furriers. Am J Ind Med 1988, 14: 187–196.

    CAS  PubMed  Google Scholar 

  100. Quirce S, Fernandez-Nieto M, de Miguel J, Sastre J: Chronic cough due to latex-induced eosinophilic bronchitis. J Allergy Clin Immunol 2001, 108: 143. 10.1067/mai.2001.116120

    CAS  PubMed  Google Scholar 

  101. Jammes Y, Delvolgo-Gori MJ, Badier M, Guillot C, Gazazian G, Parlenti L: One-year occupational exposure to a cold environment alters lung function. Arch Environ Health 2002, 57: 360–365.

    PubMed  Google Scholar 

  102. Korn RJ, Dockery DW, Speizer FE, Ware JH, Ferris BGJ: Occupational exposures and chronic respiratory symptoms. A population-based study. Am Rev Respir Dis 1987, 136: 298–304.

    CAS  PubMed  Google Scholar 

  103. Krzyzanowski M, Jedrychowski W: Occupational exposure and incidence of chronic respiratory symptoms among residents of Cracow followed for 13 years. Int Arch Occup Environ Health 1990, 62: 311–317. 10.1007/BF00640839

    CAS  PubMed  Google Scholar 

  104. Krzyzanowski M, Kauffmann F: The relation of respiratory symptoms and ventilatory function to moderate occupational exposure in a general population. Results from the French PAARC study of 16,000 adults. Int J Epidemiol 1988, 17: 397–406.

    CAS  PubMed  Google Scholar 

  105. Sunyer J, Kogevinas M, Kromhout H, Anto JM, Roca J, Tobias A, Vermeulen R, Payo F, Maldonado JA, Martinez-Moratalla J, Muniozguren N: Pulmonary ventilatory defects and occupational exposures in a population-based study in Spain. Spanish Group of the European Community Respiratory Health Survey. Am J Respir Crit Care Med 1998, 157: 512–517.

    CAS  PubMed  Google Scholar 

  106. Viegi G, Prediletto R, Paoletti P, Carrozzi L, Di Pede F, Vellutini M, Di Pede C, Giuntini C, Lebowitz MD: Respiratory effects of occupational exposure in a general population sample in north Italy. Am Rev Respir Dis 1991, 143: 510–515.

    CAS  PubMed  Google Scholar 

  107. American Thoracic Society Statement: Occupational Contribution to the Burden of Airway Disease Am J Respir Crit Care Med 2003, 167: 787–797. 10.1164/rccm.167.5.787

  108. Groneberg DA, Fischer A: Occupational Medicine and Toxicology. J Occup Med Toxicol 2006, 1: 1. 10.1186/1745-6673-1-1

    PubMed Central  Google Scholar 

  109. Groneberg DA, Welker P, Fischer TC, Dinh QT, Grutzkau A, Peiser C, Wahn U, Henz BM, Fischer A: Down-regulation of vasoactive intestinal polypeptide receptor expression in atopic dermatitis. J Allergy Clin Immunol 2003, 111: 1099–1105. 10.1067/mai.2003.1477

    CAS  PubMed  Google Scholar 

  110. Rubio-Aliaga I, Frey I, Boll M, Groneberg DA, Eichinger HM, Balling R, Daniel H: Targeted disruption of the peptide transporter Pept2 gene in mice defines its physiological role in the kidney. Mol Cell Biol 2003, 23: 3247–3252. 10.1128/MCB.23.9.3247-3252.2003

    CAS  PubMed Central  PubMed  Google Scholar 

  111. Eynott PR, Xu L, Bennett BL, Noble A, Leung SY, Nath P, Groneberg DA, Adcock IM, Chung KF: Effect of an inhibitor of Jun N-terminal protein kinase, SP600125, in single allergen challenge in sensitized rats. Immunology 2004, 112: 446–453. 10.1111/j.1365-2567.2004.01887.x

    CAS  PubMed Central  PubMed  Google Scholar 

  112. Groneberg DA, Eynott PR, Doring F, Thai Dinh Q, Oates T, Barnes PJ, Chung KF, Daniel H, Fischer A: Distribution and function of the peptide transporter PEPT2 in normal and cystic fibrosis human lung. Thorax 2002, 57: 55–60. 10.1136/thorax.57.1.55

    CAS  PubMed Central  PubMed  Google Scholar 

  113. Eynott PR, Paavolainen N, Groneberg DA, Noble A, Salmon M, Nath P, Leung SY, Chung KF: Role of nitric oxide in chronic allergen-induced airway cell proliferation and inflammation. J Pharmacol Exp Ther 2003, 304: 22–29. 10.1124/jpet.102.040295

    CAS  PubMed  Google Scholar 

  114. Dinh QT, Groneberg DA, Mingomataj E, Peiser C, Heppt W, Dinh S, Arck PC, Klapp BF, Fischer A: Expression of substance P and vanilloid receptor (VR1) in trigeminal sensory neurons projecting to the mouse nasal mucosa. Neuropeptides 2003, 37: 245–250. 10.1016/S0143-4179(03)00065-9

    CAS  PubMed  Google Scholar 

  115. Dinh QT, Groneberg DA, Peiser C, Springer J, Joachim RA, Arck PC, Klapp BF, Fischer A: Nerve growth factor-induced substance P in capsaicin-insensitive vagal neurons innervating the lower mouse airway. Clin Exp Allergy 2004, 34: 1474–1479. 10.1111/j.1365-2222.2004.02066.x

    CAS  PubMed  Google Scholar 

  116. Groneberg DA, Peiser C, Dinh QT, Matthias J, Eynott PR, Heppt W, Carlstedt I, Witt C, Fischer A, Chung KF: Distribution of respiratory mucin proteins in human nasal mucosa. Laryngoscope 2003, 113: 520–524. 10.1097/00005537-200303000-00023

    CAS  PubMed  Google Scholar 

  117. Bakke P, Eide GE, Hanoa R, Gulsvik A: Occupational dust or gas exposure and prevalences of respiratory symptoms and asthma in a general population. Eur Respir J 1991, 4: 273–278.

    CAS  PubMed  Google Scholar 

  118. Xu X, Christiani DC: Occupational exposures and physician-diagnosed asthma. Chest 1993, 104: 1364–1370.

    CAS  PubMed  Google Scholar 

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Acknowledgements

We would like to thank Prof. D. Schneider for helpful discussions. This study was supported in part by the German Research Community, and the European Union (Biomed 2, EUBMH4CT960569)

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  1. Division of Allergy Research, Otto-Heubner-Centre, Charité School of Medicine, Free University and Humboldt-University, 13353, Berlin, Germany

    David A Groneberg & Axel Fischer

  2. Institute and Outpatient Clinics for Occupational and Environmental Medicine, University of Munich, 80336, Munich, Germany

    Dennis Nowak

  3. Institute of Occupational Medicine, University of Lübeck, 23538, Lübeck, Germany

    Anke Wussow

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  1. David A Groneberg
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Groneberg, D.A., Nowak, D., Wussow, A. et al. Chronic cough due to occupational factors. J Occup Med Toxicol 1, 3 (2006). https://doi.org/10.1186/1745-6673-1-3

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Journal of Occupational Medicine and Toxicology

ISSN: 1745-6673