4.1. Interpretation of Results in Context of Available Evidence
To our knowledge, this is the first report of a cohort assessing the relationship between several types of insulating materials and non-malignant respiratory conditions among insulators. In this study, we observed that all insulating materials, except aerogels and mineral fibers, were associated with an increased probability of chest infections, while only asbestos exposure was marginally associated with higher prevalence of COPD. No association was found between insulating materials and the prevalence of asthma.
In our study, asbestos was significantly associated with a higher prevalence of repeated chest infections. Although literature emphasizing chest infections as a result of asbestos exposure is scanty, it has been reported that exposure to asbestos may increase the risk of pneumonia [30
]. We found asbestos to be associated with COPD both in single and multi-exposure models. Our observations largely resonate with previous findings where progressive lung function decline and COPD have been reported in workers with history of asbestos exposure [10
]. The significant association between asbestos and COPD in a multi-exposure model (as we did not observe any collinearity between exposures, VIF < 3) can also be explained by the fact that asbestos may cause airflow limitation in the presence of other materials, vapors, gases, or dusts, as occurs in the real world of insulating material application [34
]. However, more clinical epidemiological studies, especially longitudinal studies, are required to understand the relationship between asbestos exposure and chronic airway disease. Human biomonitoring could be applied through specific biomarkers of exposure and/or detection of early effects to assess potential health risks associated with recent exposure to insulating materials including asbestos.
The association between aerogels and all respiratory conditions towards null is plausible since aerogels appear to impose lesser health risks than any other materials used in insulation. Although the Occupational Safety and Health Agency (OSHA) described aerogels as a plausible irritant of the skin and upper airways [19
], epidemiological and mechanistic studies on the plausible health effects of aerogels are scarce. Conversely, hybrid organic–inorganic aerogels are now being considered as a promising agent for targeted drug delivery, wound healing, and bone regeneration [35
]. Therefore, whether aerogels impart beneficial or detrimental health effects needs to be understood through properly designed experimental and epidemiological research.
We also observed a significant association between exposure to calcium silicate and recurrent chest infections. Although evidence on whether calcium silicate as a standalone exposure is associated with respiratory damage is not well reported, it has been shown that calcium silicate is the principal component of wollastonite, a naturally occurring mineral often used as building and plastic industries [38
], and silicate fibers of wollastonite might impose respiratory hazards [38
]. Wollastonite has been reported to accelerate inflammatory responses in alveolar macrophages and pneumocytes, both in vivo
and in vitro
], and presumably increases the risk of infection. However, despite a plausible link between calcium silicate and the risk of fibrosis, an association of calcium silicate with airway obstruction has not been reported yet. While we observed an inverse association between calcium silicate exposure and COPD, this association did not persist after excluding those in the 4th quartile of age, as discussed above. An earlier study showed lung function decline among wollastonite-exposed workers who developed fibrosis that was greater than those who did not have fibrotic plaques [40
]. However, any association of calcium silicate exposure with lung function decline has not been demonstrated so far. Future cohorts should be considered to assess the long-term respiratory impact of calcium silicate exposure.
Similar to asbestos and calcium silicate, we also observed significant association between exposure to carbon fibers and recurrent chest infections. This is a novel finding as engineered carbon fibers used in the insulation process have not been reported to cause any respiratory illnesses to date. However, one potential mode by which respiratory illnesses could occur may be through the generation of carbon nanotubes (CNTs) during processing of those fibers, and CNTs have been reported to increase susceptibility to microbial infections in the respiratory tract [41
]. One animal study has shown that exposure to CNTs may impede with bacterial clearance from lungs and also increase the risk of infection [43
], while another has shown alteration of pulmonary macrophage function due to CNTs in experimental COPD models [44
]. However, no human studies on this topic have been reported. It must be remembered that exposure to carbon fibers may not necessarily be equivalent to CNT exposure, so results from animal studies should be interpreted cautiously.
We found a strong association between exposure to fiberglass and repetitive chest infections, and there was also a clinically important association between mineral fibers and chest infections, albeit the association was not statistically significant. Several articles have described potential health effects of mineral fibers [23
]; however, only a handful number of reports clearly described its relationship with chest infections [48
]. It has been observed that development of pneumonia among workers with a history of mineral fiber exposure could be a direct consequence of such exposure [31
], as these fibers impart detrimental effects on the natural functioning of the airway macrophages [49
]. Most of the studies related to mineral fibers have focused on fibrosis and other interstitial consequences, whereas their association with lung function or airway diseases have mostly remained unearthed. We found no association between fiberglass/mineral fibers and COPD or asthma, which is in line with the findings of the only available study where an association between fiberglass exposure and FEV1
was found in a group of workers that maintained normal lung function, and no association was found between fiberglass and COPD or asthma [21
]. More longitudinal occupational exposure studies are required to explore plausible effects of exposure to various mineral fibers on lung function changes.
Moreover, in the case of RCF exposure, we determined a significant association with recurrent chest infections. This is possibly because of the deleterious effects of man-made vitreous fibers (MMVFs) on the immune cells of the lungs [49
], thus making lungs prone to infections. However, no epidemiological or mechanistic studies are available that might help us understand the link between RCFs and chest infections. We did not observe any association between RCFs and COPD or asthma in our study. Association between RCFs and lung function decline has been mixed in previous results; however, a majority of the studies did not observe any clinically significant decline in lung function in RCF-exposed workers [50
], and those that reported RCF-associated decline in lung function were either influenced by smoking [52
], high cumulative exposure [53
], or both [52
]. Nevertheless, no study has reported any link between RCFs and clinically confirmed airway diseases, such as COPD and asthma.
4.3. Strengths and Limitations
One of the major strengths of this study lies in its approach in considering a wide range of materials used in insulation that helps in comprehending the exposure scenario of workers. Secondly, we performed several secondary analyses to test the plausible involvement of any other factors in the association between exposures and respiratory illnesses, which substantiate the robustness of our analytical methods and findings.
The limitations of this study should also be kept in mind. This is a cross-sectional study; therefore, we could not determine any causal association. However, our results are substantiated by previous epidemiological evidence, particularly related to asbestos and refractory ceramic fibers in association with respiratory complications. Despite taking into account a wide variety of insulating materials, we could not measure actual workplace exposures. Secondly, we could not measure the level of exposure to each insulating material, and participants were also unable to recollect the exact duration of exposure to each of these materials over many years; therefore, a cumulative exposure index was not achievable. Moreover, an assessment of individual exposures separately could have provided more information about their potential toxicity. However, the application of material-specific experiments would be impossible to carry out in occupational exposure studies, particularly where workers are exposed to a wide range of materials in their work. Information about PPEs was inadequate; thus, we could not assess the efficacy of PPE usage. However, based on our analyses (see Tables S2–S4
), it can be assumed that the PPEs employed by workers, which may have been inconsistently used, did not provide substantial protection for workers from exposures. Moreover, information about residual confounding, such as other plausible workplace exposures including vapor, dust, gas and fumes (VDGFs), physical and chemical agents, or socioenvironmental triggers (such as indoor conditions of the workers, environmental pollen concentration, among others), were not available and need to be considered in future studies.