Work related decrement in pulmonary function in silicon carbide production workers.
The relation between pulmonary function, cigarette smoking, and exposure to mixed respirable dust containing silicon carbide (SiC), hydrocarbons, and small quantities of quartz, cristobalite, and graphite was evaluated in 156SiC production workers using linear regression models on the difference between measured and predicted FEV1 and FVC. Workers had an average of 16 (range 2-41) years of employment and 9.5 (range 0.6-39.7) mg-year/m3 cumulative respirable dust exposure; average dust exposure while employed was 0.63 (range 0.18-1.42) mg/m3. Occasional, low level (less than or equal to 1.5 ppm) sulphur dioxide (SO2) exposure also occurred. Significant decrements in FEV1 (8.2 ml; p less than 0.03) and FVC (9.4 ml; p less than 0.01) were related to each year of employment for the entire group. Never smokers lost 17.8 ml (p less than 0.02) of FEV1 and 17.0 (p less than 0.05) of FVC a year, whereas corresponding decrements of 9.1 ml (p = 0.12) in FEV1 and 14.4 ml (p less than 0.02) in FVC were found in current smokers. Similar losses in FEV1 and FVC were related to each mg-year/m3 of cumulative dust exposure for 138 workers with complete exposure information; these findings, however, were generally not significant owing to the smaller cohort and greater variability in this exposure measure. Never smokers had large decrements in FEV1 (40.7 ml; p less than 0.02) and FVC (32.9 ml; p = 0.08) per mg-year/m3 of cumulative dust exposure and non-significant decrements were found in current smokers (FEV1: -7.1 ml; FVC: -11.7 ml). A non-significant decrement in lung function was also related to average dust exposure while employed. No changes were associated with SO(2) exposure or and SO(2) dust interaction. These findings suggest that employment in SiC production is associated with an excessive decrement in pulmonary function and that current permissible exposure limits for dusts occurring in this industry may not adequately protect workers from developing chronic pulmonary disease.
Osterman
J W
JW
Department of Environmental Science and Physiology, Harvard School of Public Health, Boston, Massachusetts, USA.
Greaves
I A
IA
Smith
T J
TJ
Hammond
S K
SK
Robins
J M
JM
Thériault
G
G
D000328:Adult; D000395:Air Pollutants, Occupational / Q000009:adverse effects*; D002244:Carbon / Q000009:adverse effects*; D017554:Carbon Compounds, Inorganic; D004651:Employment; D005541:Forced Expiratory Volume; D006801:Humans; D008168:Lung / Q000503:physiopathology*; D008297:Male; D009784:Occupational Diseases / Q000209:etiology* / Q000503:physiopathology; D012120:Respiration Disorders / Q000209:etiology* / Q000503:physiopathology; D012825:Silicon / Q000009:adverse effects*; D017655:Silicon Compounds; D012907:Smoking; D013997:Time Factors; D014797:Vital Capacity
D000395:Air Pollutants, Occupational; D017554:Carbon Compounds, Inorganic; D017655:Silicon Compounds; D002244:Carbon; C022088:silicon carbide; D012825:Silicon