DISCUSSION
As pointed out by Murray and coworkers (4) and Seaton and Cherrie (5), it is biologically plausible that the presence of lymph node fibrosis impairs the elimination of silica dust from the lungs, leading to higher lung burdens of silica and thereby increasing the likelihood of lung damage and parenchymal silicosis. In Seaton and Cherrie’s two case reports (5), both developed silicosis in the hilar lymph nodes before silicosis of the lung parenchyma. One case had a low level exposure for 30 years which led to silicotic fibrosis of the hilar lymph nodes. He then had high silica exposure for about six years and died of rapidly progressive diffuse silicotic fibrosis. The other case had the same high silica exposures as case 1 for six years, which led to fibrosis and calcification of his hilar nodes, at which point early massive parenchymal fibrosis developed.
In a cross-sectional study, evidence suggesting that lymph node silicosis may precede parenchymal silicosis in individuals may be revealed by comparing the distribution of the two types of silicosis in the sample. Murray et al (4) found 88% of their subjects with parenchymal silicosis had accompanying lymph node fibrosis. In our sample of subjects we found a very similar relationship, with 90% of subjects with parenchymal silicosis having accompanying lymph node fibrosis. Stated another way, Murray et al. (4 ) found that prevalence of parenchymal silicosis was over five times more common in those with lymph node silicosis (43.3%) than in those without lymph node silicosis (7.9%), whereas our results showed a comparable six-fold difference (66.4% and 10.1%, respectively). In our study, isolated parenchymal silicosis was much less prevalent than isolated lymph node silicosis (4% and 20%, respectively), consistent with findings reported by Murray et al. (4) where 3% and 32% had isolated parenchymal and isolated lymph node silicosis respectively. Consistent with these findings, silicosis grade for both parenchymal and lymph node silicosis tended to be most severe, those with lymph node silicosis only tended to be intermediate, and those with parenchymal silicosis were least severe. Although the temporal sequence cannot be elucidated in a cross-sectional study, these patterns of distribution between the two sites of silicosis are consistent with lymph node silicosis in general preceding parenchymal silicosis.
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Since we had silica exposure estimates, we could extend the work of Murray et al. (4). We found that subjects with lymph node silicosis only had lower cumulative and average silica exposures than those with both lymph node and parenchymal silicosis. Furthermore comparing the proportions of miners with lymph node silicosis only to those with both lymph node and parenchymal silicosis, we a higher proportion of miners with lymph node silicosis only in the two lower quartiles of cumulative silica exposure, but a higher proportion of miners with both lymph node and parenchymal silicosis in the two higher quartiles of cumulative silica exposure. These results were consistent with those of Murray et al. (4) who showed similar trends for these two groups with increasing duration of silica exposure. This result also is consistent with lymph node silicosis preceding the development of parenchymal silicosis.
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Finally, assuming this temporal relationship, in models with parenchymal silicosis as the outcome variable, we found that the presence of lymph node silicosis was a risk for the presence of parenchymal silicosis over and above the risk due to silica exposure. This may point to the importance of the hilar lymph nodes in the clearance of silica from the lungs and the additional risk for parenchymal silicosis when this mechanism is impaired.
Strengths of this study include: 1) use of detailed exposure information from work histories and industrial hygiene data, interpreted by three industrial hygienists who were familiar with the mining conditions; 2) availability of pathologic tissue specimens from a relatively large number of silica-exposed miners; 3) incorporation of independent histopathologic assessments of lymph node and parenchymal silicosis by four pathologists using agreed upon criteria.
Limitations of this study include its cross-sectional design, the limited number of subjects in particular subgroups, possible imprecision or inaccuracy in measures of silica exposure, and having smoking information on only about half of the miners. The cross-sectional study design precludes inferences regarding causality. It is also possible that the processes involved in lymph node and parenchymal silicosis are separate and independent. If development of lymph node silicosis is a more acute response to silica dust exposure and parenchymal silicosis develops after a longer duration of exposure, one could also expect lymph node silicosis to predict parenchymal silicosis. It could also be that the lymph nodes demonstrate a higher prevalence of silicosis because they either receive a higher concentration of the dust or are more sensitive to it than the parenchyma. It is clear that a cross-sectional study design cannot discern the reason for a higher prevalence of lymph node silicosis than parenchymal silicosis. The unusually low prevalence of isolated parenchymal silicosis in our study subjects contributes to some statistical instability of the estimates involved and yet is also consistent with the occurrence of parenchymal silicosis after lymph node silicosis has already developed. Respirable particles count data derived from the use of the konimeter has limitations. Only short term air samples can be taken; and the samples must be examined using optical microscopy, which may be unreliable, especially with high dust concentrations. If silica exposure estimates were imprecise or inaccurate, it is possible that adjustment for exposure could be incomplete; however, silica exposure levels were notably different in the expected direction across the four groups of individuals with and without lymph node and parenchymal silicosis. Although smoking history was only available in a subset (53%), when analyses were restricted to those with smoking habits and adjustment for smoking was performed, associations were essentially unchanged.
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An interesting aspect of our models was that the years since last exposure was significantly and positively associated with the presence of parenchymal silicosis, as was found by Kreiss and Zhen (10) in their cross-sectional study on the risk of silicosis in a Colorado mining community. Our odds ratios for years since last exposure in the various models were 1.4 and 1.5 for an increase in 10 years, while Kreiss and Zhen (10) found comparable yet slightly higher odds ratios of 1.7 to 2.4. These similarities are remarkable considering the differences in the study populations and that we used histologic evidence of silicosis while Kreiss and Zhen (10) used radiologic evidence. Although prospective studies on onset of silicosis in silica exposed workers after leaving employment would be useful, our findings further support the suggestion that lifetime follow-up is necessary to assess the full health burden of silica dust exposure.
If indeed lymph node silicosis can precede parenchymal silicosis and occur at lower silica exposures, as is suggested by our results, current methods of surveillance for silicosis, which concentrate primarily on parenchymal silicosis might miss early cases of silicosis in which the lymph nodes alone are affected. In the two cases reported by Seaton and Cherrie (5), early chest radiographs had shown hilar lymph node enlargement or fibrosis and calcification before lung involvement. Baldwin and colleagues (11) also reported on five workers exposed to silica who had chest radiographs showing enlarged hilar lymph nodes without radiographic evidence of parenchymal silicosis. They discuss that sarcoidosis is a major differential diagnosis to be considered. Thus signs of enlarged hilar lymph nodes on chest radiographs during surveillance for silicosis should raise the level of suspicion of possible early signs of effects of silica exposure. Additionally, epidemiologic studies of silicosis and lung cancer may underestimate the risk of lung cancer if parenchymal silicosis alone is considered. This is particularly true if, as hypothesized, lymph node silicosis impedes not only the clearance of silica from the lung, but other carcinogens as well.
In summary, we found that the presence of lymph node silicosis was associated with the presence of parenchymal silicosis over and above the association with silica exposure. Findings from the current study indicated that the likelihood of parenchymal silicosis was 10 times greater in those with lymph node silicosis than in those without, and this likelihood was reduced to approximately 6 times greater after adjusting for silica exposure. Results from Murray et al. (4) showed a similar yet slightly greater reduction in ORs from 8.9 to 2.6 with adjustment for duration of silica exposure. These results are consistent with the potentially important role of hilar lymph nodes in the clearance of silica from the lungs and may also reflect an additional risk for parenchymal silicosis when this mechanism is impaired.
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