NYC-WTC_000195068

NYC 9/11 Public Portal Document

AJjBESTOS MEDITEXT ® - Medical Management Page 6 of 15

A. IMMUNE SYSTEM DISORDER 1. COMPLEMENT ACTIVATION - Asbestos activates complement by an alternative pathway, resulting in leukocyte concentration and lysosomal enzyme release (Dark & Pingleton, 1983). a. With activation of the alternative complement pathway, C5a cleavage product is generated, which serves as a chemotactic agent for alveolar macrophages (Kagan, 1988). 2. CELLULAR/HUMORAL IMMUNOLOGIC CHANGES - Reports of serum abnormalities have not been consistent (Nash et al, 1981). Despite some variability, most studies indicate that cell-mediated immunity can be depressed (ATSDR, 1995; Weill & Hughes, 1988). Asbestos, especially chrysotile, can suppress natural killer cell activity and thus interfere with the recognition and destruction of malignant cells (Robinson, 1989). a. Other studies have reported increased cellular immune responses (Anton-Culver et al, 1988; Delclos et al, 1989). b. Elevated bronchoalveolar T4/T8 lymphocyte ratios were noted in 32 subjects with significant asbestos exposure (Delclos et al, 1989). c. Shipyard workers with radiographically detectable asbestosis had greater numbers of T helper and T suppressor cells (disproportionately more of the latter) compared to blood donor controls (Anton-Culver et al, 1988). Increased pokeweed mitogen stimulation was also noted. d. Differences in humoral immune response have also been reported (Anton-Culver et al, 1988; ATSDR, 1995; Talcott & Antman, 1988; Weill & Hughes, 1988). e. Elevated carcinoembryonic antigen levels have been identified with colorectal cancers, but the clinical relevance of elevated immunoglobulins and other serum proteins have yet to be determined (Talcott & Antman, 1988). f. Autoantibodies (rheumatoid factor, antinuclear antibodies) are typically abnormally high in asbestos-exposed workers (ATSDR, 1995; Weill & Hughes, 1988). Caplan's syndrome (pneumoconioses with rheumatoid changes) has been noted in asbestos workers which can lead to rheumatoid arthritis (ATSDR, 1995). In a retrospective study of 109 environmentally-exposed persons, those with pleural plaques had an increased incidence of antinuclear antibodies, as well as increased IgA levels (Zerva et al, 1989). g. Increased levels of anti-double strand DNA antibodies were seen in persons occupationally exposed to asbestos, compared with a non-exposed group (Marczynski et al, 1994). h. Higher IgG and IgA levels were noted among shipyard workers with radiographically detected asbestosis (Anton-Culver et al, 1988). Higher IgG and IgA levels were also noted in environmental (nonoccupational) asbestos exposures. The pressure of pleural plaques accentuated the effect on humoral immunity (Zerva et al, 1989). B. INFECTION 1. PREDISPOSITION TO INFECTION - Bronchiectasis and unexplained (but commonly encountered) immunologic deficiencies can predispose an asbestotic patient to infections, including tuberculosis (Baris et al, 1988; Finkel, 1983). Infection can cause further progressive fibrosis, which leads to cor pulmonale.

3.20 REPRODUCTIVE HAZARDS

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