Mill workers

If disease is mediated by non-specific activation of the alternative pathway, it does not explain why some mill workers, who are presumably exposed to equal dust levels, do not develop symptoms. One possible explanation is that there is host factor variability, such as end-organ sensitivity. It has also been proposed that pre-existing, non-specific bronchial hyperreactivity may be Important in development of byssinosis (51), but, to date, there is little evidence for this hypothesis (52- ). 

It is not known if platelets are actually involved in bysslnosis however, a reduction of platelets has been shown in cotton mill workers on the first day of the work week (118). 

Mean Immunoglobulin Concentrations in Sera of Byssinotic and Non-Byssinotic Cotton Mill Workers At Different Time Intervals... 

Our data showing normal serum complement levels in cotton mill workers (normal and byssinotic) does not support a complement activation mechanism for the pathogenesis of byssinosis, but the data does not eliminate the possiblity of complement activation in the etiology of byssinosis (Table V). As complement activation is a local reaction, small amounts of complement fragments sufficient... 

Clinical studies of cotton mill workers who had previously demonstrated a decreased expiratory flow measured by flow volume curves and FEV during cotton dust exposure showed an increase in WBC to 25.5% after 4 hours of exposure. Segmented neutrophils increased most (33%), while eosinophil mean counts did not change. The ratio of segmented neutrophils to epithelial cells from nasal mucosal swabs increased from 0.56 before to 1.84 after 4 hours of exposure. Peripheral blood and PMN counts increased upon exposure to cotton dust, and PMN were recruited to the nasal mucosa. Chest tightness and decreased flow were temporarily correlated with leukocyte recruitment following cotton dust exposure (2). 

As the major clinical manifestation of the acute byssinotic reaction is a drop in FEV, it is interesting to speculate that the bronchoconstriction observed in cotton mill workers may be in part or in full the result of constrictor substances in inhaled cotton dust. 

If the receptors involved in the acute byssinotic reaction can be determined, pharmacologic blocking agents may be used to treat affected cotton mill workers or, conversely, preprocessing of cotton to eliminate the constrictor might prove feasible. 

Tuffnell in 1960 (19) reported one bysslnotlc cotton mill worker who reacted to a dust prepared from the leaves and bracts of cotton plants and had a similar reaction (symptoms and a fall in maximal breathing capacity) to mill dust but no reaction to exposure to a dust containing Bacillus pumllls. Three byssinotlc workers did not react to dusts of gram-positive bacteria or fungi but did react to dust from leaves of cotton plants (19). He concluded that there was no relation between total numbers of bacteria or fungi present in the air and the prevalence of byssinosls. 

A deficiency of niacin in the diet results in the disease known as pellagra, characterized by the four D s diarrhea, dermatitis, dementia, and death. In the early years of the twentieth century in the United States, pellagra was common among poor tenant farmers and mill workers in the rural South. The diet there at that time was rich in com that contained little niacin and little available tryptophan from which to synthesize it. 

Cartier, P. (1955). Some clinical observations of asbestosis in mine and mill workers. AMA Arch Ind. Health 11 204—207. 

Some studies of survivors of massive chlorine exposures have shown either persistent obstructive or restrictive deficits, but pre-exposure data on these patients were not available. Persistent respiratory symptoms, bronchial obstruction, and bronchial hyperresponsiveness were observed in 82%, 23%, and 41 % of chronically exposed pulp mill workers, respectively, 18-24 months after cessation of exposure." In most cases it is not known whether prolonged symptoms after chlorine exposure are due to aggravation of preexisting conditions such as tuberculosis, asthma, chronic obstructive pulmonary disease, or heart disease." "... 

Harris TR, Merchant JA, Kilburn KH, Hamilton JD Byssinosis and respiratory diseases of cotton mill workers, jf Occup Med 14 199-206, 1972... 

Three pulp mill workers died after inhalation of fumes for approximately 10-15 minutes from a nitric acid tank explosion (concentrations not available). No significant respiratory complaints were apparent during initial examination. However, 4—6 hours later they became cyanotic with frothy fluid escaping from the nose and mouth. All died in less than 24 hours. Necropsy showed bronchiolar epithelial necrosis, marked capillary engorgement, and slight interstitial edema of alveoli the lungs were five times heavier than normal and released abundant frothy fluid from all lobes. The delayed manifestations of lung injury were consistent... 

Hajela R, Janigan DT, Landrigan PL, et al Fatal pulmonary edema due to nitric acid fume inhalation in three pulp-mill workers. Chest 91 487-489, 1990... 

In a group of uranium mill workers, there was an excess of deaths from malignant disease of lymphatic and hematopoietic tissue data from animal experiments suggested that this excess may have resulted from irradiation of lymph nodes by thorium-230, a disintegration product of uranium. Some absorbed uranium is deposited in bone. A potential risk of radiation effects on bone marrow has been postulated, but extensive clinical studies on exposed workers have disclosed no hematologic abnormalities. ... 

Archer VE, Wagoner JK, Lundin FE Jr Cancer mortality among uranium mill workers, y Occup Med 15 11-14, 1973... 

A significantly (p<0.05) increased incidence of malignancies in the lymphatic and hematopoietic tissues of uranium mill workers (cohort of 662 males) was found by Archer et al. (1973). The radioactivity in the tracheobronchial lymph nodes of the workers was found to be primarily the result of alpha emissions from thorium-230 and not from uranium-234 or uranium-238. Consequently, the authors suggested that the increased incidence of malignancies may have been a result of thorium-230 exposure and not uranium exposure. Exposure levels of thorium were not reported therefore, the results of the study are not reported on Table 2-1 or plotted in Figure 2-1. 

After inhalation exposure, the primary route of excretion is in the feces following ciliary clearance from the lungs to the gastrointestinal tract (Wrenn et al. 1981). Fecal excretion may account for as much as 97% of total excretion (Fisher et al. 1983). Higher levels of thorium-230 were excreted in the feces by active crushermen (uranium mill workers exposed to uranium ore dust in the crusher building) compared to retired workers or controls (Fisher et al. 1983). Levels of thorium-230 in the urine were comparable to those of retired workers, and the levels in both were significantly greater than controls. 

Band PR, Le ND, Fang R, et al. 1997. Cohort mortality study of pulp and paper mill workers in British Columbia, Canada. Am J Epidemiol 146(2) 186-194. 

Kennedy SM, Enarson DA, Janssen RG, et al. 1991. Lung health consequences of reported accidental chlorine gas exposure among pulp mill workers. Am Rev Respir Dis 143(l) 74-79. 

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