John E. Diem

Humoral immunologic abnormalities in workers exposed to asbestos cement dust

Serum specimens from 144 workers exposed to asbestos cement dust were examined for the presence of ANA, RF, immunoglobulins, and IC. These immunologic findings were compared with chest radiographic changes. A high percentage of workers had polyclonal hypergammaglobulinemia, and there was a statistically significant association between elevated levels of IgG and IgM and radiographic classification. Although a significant number of workers had an increased prevalence of ANA and elevated levels of IC, there was no correlation between these parameters and chest radiographs. These findings support B cell hyperactivity in workers exposed to asbestos and suggest that autoantibody production and IC are not directly involved in disease pathogenesis.

Evaluation of dust exposure in asbestos cement manufacturing operations

Previous investigations of the health of workers of the asbestos cement industry have demonstrated dose-response relationships for the diffuse radiographic changes of asbestosis and pulmonary function impairment. Studies of the mortality experience of past employees have also identified levels of cumulative exposure above which an excess of respiratory cancer could be detected. These epidemiologic studies were based on particulate concentrations determined by the midget impinger. We attempted to develop information that might lead to conversion of particulate to fiber concentrations in the industry in order that the risk assessment could be related to the current membrane filter methods. Pairs of impinger and membrane filter samples were taken in the various areas of the plant. Personal samples were also taken to determine the current exposure of workers. The ratio of fiber concentration to particle count varied from 0.63 to 2.5. Por correlation (0.18) was obtained at low fiber and particle counts and good correlation (0.91) was demonstrated in dustry areas where asbestos and silica were handled in a dry form. The concentration of fibers in 80% of the personal samples was less than 2 fibers/cc, and 60% were less than 0.5 fibers/cc. The results also show that no one conversion factor can be used for all areas of this type of operation.

Effect of atropine on the bronchial response of asthmatic subjects to the inhalation of ultrasonically nebulized distilled water

To determine whether atropine provides protection against the bronchoconstriction that develops in asthmatic subjects after inhalation of ultrasonically nebulized distilled water, we exposed six asthmatic patients to this stimulus with and without pretreatment with atropine (0.04 mg/kg). The mean FEV1 decreased from 3.32 to 2.39 L (-28%) without and from 3.49 to 3.18 L (-9%) with atropine. This protective effect was statistically significant (p less than 0.05), suggesting that cholinergic pathways are involved in the obstructive response to the inhalation of ultrasonically nebulized distilled water.

Immunologic aberrations in asbestos cement workers: dissociation from asbestosis

Immunoregulatory disorders have been implicated in the pathogenesis of asbestosis. We therefore compared the immunologic status of a well-characterized group of 31 current and former asbestos-cement workers with that of a group of 52 healthy controls, after adjustments had been made for the possible confounding effects of age, race, and smoking. The asbestos workers had significantly decreased percentages and numbers of both B and T lymphocytes in peripheral blood and a paradoxical IgG hypergammaglobulinemia. Analysis of T-lymphocyte subpopulations revealed that total T-cell numbers (OKT3+), helper-inducer T-cell numbers (OKT4+), and suppressor-cytotoxic T cell numbers (OKT8+) were decreased by similar proportions. These decreases were negatively correlated with time elapsing since the end of exposure to asbestos. In both workers and controls, lymphocyte proliferative responses to phytohemagglutinin (PHA) were correlated positively with the number of OKT4+ cells and negatively with age and serum IgG levels. When adjustments had been made for these confounding variables, no differences in PHA responses were noted between workers and controls. No relationship was detected in the workers between any of the immunologic aberrations noted and (1) radiographic category of pneumoconiosis, (2) estimates of cumulative asbestos exposure, or (3) abnormalities of pulmonary function. These data suggest that the immunologic perturbations we have noted in asbestos-exposed individuals are epiphenomena, unrelated to the pathogenesis of asbestosis itself.

Evidence for histamine-mediated inhibition of monocyte chemotaxis in atopic dermatitis.

Leukocyte chemotaxis was studied in 11 patients with severe childhood onset atopic dermatitis at a time when their disease was relatively quiescent. Pyoderma had been an important complication of the dermatitis in these patients. The chemotactic responsiveness of patient neutrophils and monocytes was on the average not significantly different from that of healthy control subjects, although three patients were identified who had significantly impaired responses. No correlation between IgE levels and leukocyte chemotaxis was observed. Because excessive amounts of histamine have been recovered from the skin of patients with atopic dermatitis, we evaluated the effects of histamine on the chemotactic responsiveness of leukocytes from these patients. Histamine caused a small dose-related increase in chemotaxis of neutrophils from both patients and control subjects (10(-7)M to 10(-5)M histamine). In contrast, histamine had no effect on the chemotaxis of monocytes from control subjects but inhibited the chemotactic responsiveness of monocytes from atopic dermatitis patients. These findings suggest that an abnormal sensitivity of monocytes to histamine is an intrinsic feature of atopic dermatitis that may be detectable when the disease is quiescent. Furthermore, this abnormality may contribute to the impairment of monocyte chemotaxis that has been previously observed in patients with active atopic dermatitis.

Accumulation of fluoride by the soybean (Glycine max L. Merrill var Dare) part II: Accumulation in leaves, fruit, and seeds

Abstract Soybeans (Glycine max var. Dare) were exposed to hydrogen fluoride at 2.0 μg HF m‐3‐ 16.1 μg HF m‐3 during continuous and interrupted exposures of 109 days and 53 days, respectively, following development of the seventh trifoliates. Resulting patterns of accumulation and loss suggest that leaf fluoride is exchanged with the atmosphere through a catenary two compartment system. The fluoride literature was reviewed with respect to site of fluoride entry, transport, and accumulation and used to define the boundaries and exchange relationships of the compartments. The experimental data suggest that leaf injury plays an important role in accumulation by limiting the surface available for exchange. Measurement of the rate of fluoride disappearance following intermittent exposure suggests that the distribution of excretable fluoride in the leaf changes with time and leaf necrosis. Fluoride levels in leaves, fruit and seeds showed significant increases over background concentrations, with highest levels ...

Accumulation of fluoride by the soybean (Glycine max L. Merrill var Dare) part I: Visible injury and related effects on seed yield

Abstract Soybeans (Glycine max L. Merrill var Dare) showed moderate resistance to leaf chlorosis and necrosis following extended exposures (109 days) to hydrogen fluoride concentrations of 2.0 μgHFm‐3 to 16. 1μg HF m‐3, inclusive (ECt2 = 400μg HF m‐3‐d ECt50 = 1500 μg HF m‐3‐d. Seed production was reduced at the lowest level of exposure and occurred with negligible visible injury to leaves. Pack and Sulzbach (1976) have suggested that the latter may result from effects on pollen production or germination, which is supported by these findings. In addition to reduced yields, seed production in fumigated plants was significantly retarded. Delays in maturityranged from an estimated one to two weeks (at 1.0 μg HF m‐3) to 6 weeks (at 16 μg HF m‐3).